Association between short term exposure to fine particulate matter and heart rate variability in older subjects with and without heart disease.

BACKGROUND: Short term increases in exposure to particulate matter (PM) air pollution are associated with increased cardiovascular morbidity and mortality. The mechanism behind this effect is unclear, although changes in autonomic control have been observed. It was hypothesised that increases in fine PM measured at the subjects' home in the preceding hour would be associated with decreased high frequency heart rate variability (HF-HRV) in individuals with pre-existing cardiac disease. METHODS: Two hundred and eighty five daily 20 minute measures of HRV (including a paced breathing protocol) were made in the homes of 34 elderly individuals with (n = 21) and without (n = 13) cardiovascular disease (CVD) over a 10 day period in Seattle between February 2000 and March 2002. Fine PM was continuously measured by nephelometry at the individuals' homes. RESULTS: The median age of the study population was 77 years (range 57-87) and 44% were male. Models that adjusted for health status, relative humidity, temperature, mean heart rate, and medication use did not find a significant association between a 10 microg/m3 increase in 1 hour mean outdoor PM2.5 before the HRV measurement and a change in HF-HRV power in individuals with CVD (3% increase in median HF-HRV (95% CI -19 to 32)) or without CVD (5% decrease in median HF-HRV (95% CI -34 to 36)). Similarly, no association was evident using 4 hour and 24 hour mean outdoor PM2.5 exposures before the HRV measurement. CONCLUSION: No association was found between increased residence levels of fine PM and frequency domain measures of HRV in elderly individuals.

Measurement of offline exhaled nitric oxide in a study of community exposure to air pollution.

As part of a large panel study in Seattle, Washington, we measured levels of exhaled nitric oxide (eNO) in children's homes and fixed-site particulate matter with aerodynamic diameters of 2.5 micro m or less (PM(2.5)) outside and inside the homes as well as personal PM(2.5) during winter and spring sessions of 2000-2001. Nineteen subjects 6-13 years of age participated; 9 of the 19 were on inhaled corticosteroid (ICS) therapy. Exhaled breath measurements were collected offline into a Mylar balloon for up to 10 consecutive days. Mean eNO values were 19.1 (SD +/- 11.4) ppb in winter sessions and 12.5 +/- 6.6 ppb in spring sessions. Fixed-site PM(2.5) mean concentrations were 10.1 +/- 5.7 microg/m(3) outside homes and 13.3 +/- 1.4 inside homes; the personal PM(2.5) mean was 13.4 +/- 3.2 microg/m(3). We used a linear mixed-effects model with random intercept and an interaction term for medications to test for within-subject-within-session associations between eNO and various PM(2.5) values. We found a 10 microg/m(3) increase in PM(2.5) from the outdoor, indoor, personal, and central-site measurements that was associated with increases in eNO in all subjects at lag day zero. The effect was 4.3 ppb [95% confidence interval (CI), 1.4-7.29] with the outdoor monitor, 4.2 ppb (95% CI, 1.02-7.4) for the indoor monitor, 4.5 ppb (95% CI, 1.02-7.9) with the personal monitor, and 3.8 ppb (95% CI, 1.2-6.4) for the central monitors. The interaction term for medication category (ICS users vs. nonusers) was significant in all analyses. These findings suggest that eNO can be used as an assessment tool in epidemiologic studies of health effects of air pollution.

A cost-effective weighing chamber for particulate matter filters.

Particulate matter (PM) is a ubiquitous air pollutant that has been receiving increasing attention in recent years due in part to the association between PM and a number of adverse health outcomes, including mortality and increases in emergency room visits and respiratory symptoms, as well as exacerbation of asthma and decrements in lung function. As a result, the ability to accurately sample ambient PM has become important, both to researchers and to regulatory agencies. The federal reference method for the determination of fine PM as PM2.5 in the atmosphere recommends that particle-sampling filters be conditioned and weighed in an environment with constant temperature and relative humidity (RH). It is also recommended that vibration, electrostatic charges, and contamination of the filters from laboratory air be minimized to reduce variability in filter weight measurements. These controls have typically been maintained in small, environmentally controlled "cleanrooms." As an alternative to constructing an elaborate cleanroom, we have designed, and presented in this paper, an inexpensive weighing chamber to maintain the necessary level of humidity control.

Windblown dust contributes to high PM2.5 concentrations.

The revised National Ambient Air Quality Standards for PM include fine particulate standards based upon mass measurements of PM2.5. It is possible in arid and semi-arid regions to observe significant coarse mode intrusion in the PM2.5 measurement. In this work, continuous PM10, PM2.5, and PM1.0 were measured during several windblown dust events in Spokane, WA. PM2.5 constituted approximately 30% of the PM10 during the dust event days, compared with approximately 48% on the non-dusty days preceding the dust events. Both PM10 and PM2.5 were enhanced during the dust events. However, PM1.0 was not enhanced during dust storms that originated within the state of Washington. During a dust storm that originated in Asia and impacted Spokane, PM1.0 was also enhanced, although the Asian dust reached Washington during a period of stagnation and poor dispersion, so that local sources were also contributing to high particulate levels. The "intermodal" region of PM, defined as particles ranging in aerodynamic size from 1.0 to 2.5 microns, was found to represent a significant fraction of PM2.5 (approximately 51%) during windblown dust events, compared with 28% during the non-dusty days before the dust events.

Associations between air pollution and mortality in Phoenix, 1995-1997.

We evaluated the association between mortality outcomes in elderly individuals and particulate matter (PM) of varying aerodynamic diameters (in micrometers) [PM(10), PM(2.5), and PM(CF )(PM(10) minus PM(2.5))], and selected particulate and gaseous phase pollutants in Phoenix, Arizona, using 3 years of daily data (1995-1997). Although source apportionment and epidemiologic methods have been previously combined to investigate the effects of air pollution on mortality, this is the first study to use detailed PM composition data in a time-series analysis of mortality. Phoenix is in the arid Southwest and has approximately 1 million residents (9. 7% of the residents are > 65 years of age). PM data were obtained from the U.S. Environmental Protection Agency (EPA) National Exposure Research Laboratory Platform in central Phoenix. We obtained gaseous pollutant data, specifically carbon monoxide, nitrogen dioxide, ozone, and sulfur dioxide data, from the EPA Aerometric Information Retrieval System Database. We used Poisson regression analysis to evaluate the associations between air pollution and nonaccidental mortality and cardiovascular mortality. Total mortality was significantly associated with CO and NO(2) (p < 0.05) and weakly associated with SO(2), PM(10), and PM(CF) (p < 0. 10). Cardiovascular mortality was significantly associated with CO, NO(2), SO(2), PM(2.5), PM(10), PM(CF) (p < 0.05), and elemental carbon. Factor analysis revealed that both combustion-related pollutants and secondary aerosols (sulfates) were associated with cardiovascular mortality.

An association between fine particles and asthma emergency department visits for children in Seattle.

Asthma is the most common chronic illness of childhood and its prevalence is increasing, causing much concern for identification of risk factors such as air pollution. We previously conducted a study showing a relationship between asthma visits in all persons < 65 years of age to emergency departments (EDs) and air pollution in Seattle, Washington. In that study the most frequent zip codes of the visits were in the inner city. The Seattle-King County Department of Public Health (Seattle, WA) subsequently published a report which showed that the hospitalization rate for children in the inner city was over 600/100,000, whereas it was < 100/100,000 for children living in the suburbs. Therefore, we conducted the present study to evaluate whether asthma visits to hospital emergency departments in the inner city of Seattle were associated with outdoor air pollution levels. ED visits to six hospitals for asthma and daily air pollution data were obtained for 15 months during 1995 and 1996. The association between air pollution and childhood ED visits for asthma from the inner city area with high asthma hospitalization rates were compared with those from lower hospital utilization areas. Daily ED counts were regressed against fine particulate matter (PM), carbon monoxide (CO), sulfur dioxide, and nitrogen dioxide using a semiparametric Poisson regression model. Significant associations were found between ED visits for asthma in children and fine PM and CO. A change of 11 microg/m3 in fine PM was associated with a relative rate of 1.15 [95% confidence interval (CI), 1.08-1.23]. There was no stronger association between ED visits for asthma and air pollution in the higher hospital utilization area than in the lower utilization area. These findings were seen when estimated PM2.5 concentrations were below the newly adopted annual National Ambient Air Quality Standard of 15 microg/m3.

Effects of ambient air pollution on nonelderly asthma hospital admissions in Seattle, Washington, 1987-1994.

As part of the Clean Air Act, Congress has directed EPA to set air quality standards to protect sensitive population groups from air pollutants in the ambient environment. People with asthma represent one such group. We undertook a study of the relation between measured ambient air pollutants in Seattle and nonelderly hospital admissions with a principal diagnosis of asthma. We regressed daily hospital admissions to local hospitals for area residents from 1987 through 1994 on particulate matter less than 10 and 2.5 microm in aerodynamic diameter (PM10 and PM2.5, respectively); coarse particulate mass; sulfur dioxide (SO2); ozone (O3); and carbon monoxide (CO) in a Poisson regression model with control for time trends, seasonal variations, and temperature-related weather effects. With the exception of seasonally monitored O3, we supplemented incomplete pollutant measures in a multiple imputation model to create a complete time series of exposure measures. We found an estimated 4-5% increase in the rate of asthma hospital admissions associated with an interquartile range change in PM (19 microg/m3 PM(10),11.8 microg/m3 PM2.5, and 9.3 microg/m3 coarse particulate mass) lagged 1 day; relative rates were as follows: for PM10, 1.05 [95% confidence interval (CI) = 1.02-1.08]; for PM2.5, 1.04 (95% CI = 1.02-1.07); and for coarse particulate mass, 1.04 (95% CI = 1.01-1.07). In single-pollutant models we also found that a 6% increase in the rate of admission was associated with an interquartile range change in CO (interquartile range, 924 parts per billion; 95% CI = 1.03-1.09) at a lag of 3 days and an interquartile range change in O3 (interquartile range, 20 parts per billion; 95% CI = 1.02-1.11) at a lag of 2 days. We did not observe an association for SO2. We found PM and CO to be jointly associated with asthma admissions. We estimated the highest increase in risk in the spring and fall seasons.

Wood smoke: emissions and noncancer respiratory effects.

In conclusion, this review reveals much about the constituents and fate of wood smoke but not enough about the health effects. Animal toxicological studies show that wood smoke exposure can disrupt cellular membranes, depress macrophage activity, destroy ciliated and secretory respiratory epithelial cells, and cause aberrations in biochemical enzyme levels. With respect to the human epidemiological data, the literature summarized in Table 4 shows a coherence of the data from young children, with 7/8 studies especially in children with asthma, reporting increased respiratory symptoms, lower respiratory infection, and decreased pulmonary function as a result of exposure to wood smoke. As Bates (6) has discussed, coherence of the data, although not amenable to statistical tests, carries the weight of linkage and plausibility. These adverse respiratory effects associated with wood smoke exposure also comply with many of Brandon Hill's aspects of association necessary to establish causation (40). There is strength of association, consistency (7/8 studies showing positive associations), temporality, plausibility, coherence, and analogy (using ETS exposure; 70, 94). A biological gradient has not been shown, although one is suggested in the study of pulmonary function in wildfire fighters. We conclude that the preponderance of the data suggest a causal relationship between elevated wood smoke levels and adverse respiratory health outcomes in young children.

Pulmonary function changes in children associated with fine particulate matter.

During winter months many neighborhoods in the Seattle metropolitan area are heavily affected by particulate matter from residential wood burning. A study was conducted to investigate the relationship between fine particulate matter and pulmonary function in young children. The subjects were 326 elementary school children, including 24 asthmatics, who lived in an area with high particulate concentrations predominantly from residential wood burning. FEV1 and FVC were measured before, during and after the 1988-1989 and 1989-1990 winter heating seasons. Fine particulate matter was assessed using a light-scattering instrument. Analysis of the relationship between light scattering and lung function indicated that an increase in particulate air pollution was associated with a decline in asthmatic children's pulmonary function. FEV1 and FVC in the asthmatic children dropped an average of 34 and 37 ml respectively for each 10(-4) m-1 increase in sigma sp. This sigma sp increase corresponds to an increase in PM2.5 of 20 micrograms/m3. It is concluded that fine particulate matter from wood burning is significantly associated with acute respiratory irritation in young asthmatic children.

Particulate air pollution and hospital emergency room visits for asthma in Seattle.

Recent studies have associated short-term exposure to respirable particulate matter (PM10) exposure with peak flow decrements, increased symptoms of respiratory irritation, increased use of asthma medications, and increased hospitalization for asthma. Increased mortality from chronic respiratory disease has also been reported. To help confirm whether PM10 exposure is a risk factor for the exacerbation of asthma, we compiled daily records of asthma emergency room visits from eight hospitals in the Seattle area. In Poisson regressions controlling for weather, season, time trends, age, hospital, and day of the week, the daily counts of emergency room visits for persons under age 65 were significantly associated with PM10 exposure on the previous day. The mean of the previous 4 days' PM10 was a better predictor (p < 0.005). The relative risk for a 30 micrograms/m3 increase in PM10 was 1.12 (95% confidence interval 1.20 to 1.04). Daily PM10 concentrations never exceeded 70% of the current ambient air quality standards during the period. The consistency of investigations of the health effects of PM10 suggest that increased attention should be given to the control of particulate matter air pollution.

The effect of duration of exposure on sulfuric acid-induced pulmonary function changes in asthmatic adolescent subjects: a dose-response study.

To evaluate the pulmonary effects of varying doses of sulfuric acid, adolescent subjects with asthma were exposed to 35 or 70 micrograms/m3 sulfuric acid for 45 or 90 min. Exposure was carried out during intermittent moderate exercise. The pulmonary functions measured before and after exposure were FEV1, FVC, and total respiratory resistance. The 45 min exposures were associated with larger decreases in FEV1 (-6% or -3%) than the 90 min exposures (-1% or +2%). Analysis of variance of the change in FEV1 among the exposures revealed that the 45 min exposure to 35 micrograms/m3 was significant (p = 0.03). The p value for 45 min exposure to 70 micrograms/m3 was not significant (p = 0.08). Using analysis of variance, neither of the 90 min exposures was associated with a significant decrease in FEV1 compared to air exposure. Also, none of the changes in FVC or RT was significant. When baseline to post-exposure changes were compared for each of the five test atmospheres using paired t tests, both of the 45 min exposures were associated with statistical significance (p < 0.001 for 35 micrograms/m3 and p < 0.005 for 70 micrograms/m3). This baseline to post exposure change was not statistically significant for the 90 min exposures. The reason for the lesser effect on pulmonary function at increased exposure duration is not known; it may be due to changes in either varying deposition patterns or changes in buffering capacity of the cells lining the airways. With respect to individual sensitivities to H2SO4, the data showed a significant consistency across test atmospheres.

Response of young asthmatic patients to inhaled sulfuric acid.

The intent of this study was to explore the effects of inhalation of [H+] defined here as acid airborne particles at near ambient concentrations on the pulmonary function of adolescent asthmatic subjects. During rest and exercise, 22 adolescent asthmatic subjects inhaled atmospheres containing either clean air or sulfuric acid particles (H2SO4) through a mouthpiece. The concentration of hydrogen ion at the mouthpiece ([H+]) ranged from 1.18 to 3.59 mumol/m3 (51 to 176 micrograms/m3 of H2SO4). The lower range of [H+] is near the peak values measured during the summer months in the eastern United States and Canada. Pulmonary function and oral ammonia levels were measured before and after exposure in all subjects. Significant group responses to [H+] were seen in FEV1 (p = 0.016) and FVC (p = 0.039) measured 2 to 3 min post-exposure. Also, the slopes of the change in pulmonary function versus [H+] were computed for each subject. The slopes of changes in FEV1 and Vmax50 and Vmax75 versus [H+] were related to the subject's response to a standard exercise treadmill test, specifically to the subject's percentage decrease in FEV1 after exercise challenge. Pulmonary function changes 20 min postexposure did not show a significant group response to [H+] exposure; however, the relationship between percentage FEV1 decrease after exercise and the individual slopes of Vmax50 and Vmax75 persisted for at least 20 min after exposure.

A theoretical investigation of the pressure and temperature dependence of atmospheric ozone deposition to trees.

Methods for describing the exposure patterns of forests to atmospheric ozone concentrations are compared with special emphasis on the situation at high altitudes, such as the Appalachian Mountains of the eastern USA. Limitations to the use of ozone concentration as mass per unit volume are discussed and a correction for temperature and pressure changes is derived. If identical ozone mass concentrations were measured at two sites separated by 2000 m elevation, the ozone flux at the lower site would exceed the flux at the higher site by 4-8% due to temperature and pressure effects on both air volume and ozone deposition velocity. It is recommended that ozone exposures be described in terms of 'flux-corrected' mass concentrations or volumetric mixing ratios when ambient ozone data from sites at different altitudes are to be compared.

The influence of chemical and physical forms of ambient air acids on airway doses.

The effects of ambient relative humidity and particle size on acid deposition within the airways have been examined with a computer model. For H2SO4 particles initially at 90% relative humidity in ambient air that are inhaled via the nose or mouth, there is significant deposition of acid in the airways even in the presence of typical values of respiratory NH3. When these same particles are found in a fog at 100.015% relative humidity, there is significant deposition of acid in the nasal region during nose breathing but insignificant deposition to the deep lung for either nose or mouth breathing. The factors governing the partitioning of labile acid gases in the gas and liquid phases prior to inhalation are also discussed.

Measurements of respiratory ammonia and the chemical neutralization of inhaled sulfuric acid aerosol in anesthetized dogs.

The extent of neutralization of inhaled H2SO4 aerosol by endogenous NH3 has been measured in the surgically isolated upper airways of anesthetized dogs. Neutralization was observed to be inversely proportional to particle size. The H2SO4 particles with initial dry diameters of 0.5 micrometer and 1.0 micrometer underwent 0.28 (+/- 0.08) and 0.06 (+/- 0.06)% neutralization per ppb of laryngeal NH3, respectively, during passage through the mouth and out of the larynx at a flow of 0.1 L/s. At either particle size, neutralization is related to the route of entry, being greater for entry via the mouth than the nose. Limited measurements for entry via the mouth show more neutralization of 0.7 micrometer particles at 0.1 L/s than at 0.2 L/s. These results are consistent with a reaction that is limited by the rate of NH4 diffusion to the particle's surface.

A method for continuous measurement of ammonia in respiratory airways.

A method has been developed that can continuously measure respiratory NH3 with a detection limit of 30 parts per billion by volume (ppbv) at an averaging time of 1 s. The method is based on the chemiluminescent detection of NO, which is produced by oxidizing NH3 at 850 degrees C. A polyethylene sampling probe, incorporating a heated capillary tip bathed in dry, NH3-free diluent air, minimizes NH3 losses due to absorption in breath condensate. In one subject, flow and tidal volume were monitored during quiet mouth breathing while NH3 and CO2 were sampled at the lips. In 10 subjects, NH3, and CO2 were sampled at the lips during quiet mouth breathing ranged from 280 to 1,280 ppbv (mean plus or minus SE, 540 PLUS OR MINUS 85 PPBV).

Ammonia in the human airways: neutralization of inspired acid sulfate aerosols.

In the human being, expired ammonia concentrations from 7 to 520 micrograms per cubic meter are controlled by the last airway segment traversed by the air, and such concentrations are higher in the mouth than nose. Inspired submicrometric sulfuric acid aerosol at a mass concentration of 600 +/- 100 micrograms per cubic meter was found to be an ammonium salt with an average ammonium to sulfate molar ratio of greater than or equal to 1, when sampled within 0.5 second after exhalation.