Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Pollution”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 901 records · Page 50Linked to original sources
PubMed1996

Airway response of asthmatic subjects to inhaled allergen after exposure to pollutants.

BACKGROUND: Recent studies have suggested that air pollutants resulting from vehicle exhaust emissions and burning of fossil fuels, either in combination or individually, may enhance the airway response of asthmatic subjects to inhaled allergen. It was hypothesised that the airway response to inhaled allergen after exposure to a combination of 400 ppb nitrogen dioxide (NO2) and 200 ppb sulphur dioxide (SO2) is increased 24-48 hours after exposure. METHODS: Thirteen mild atopic asthmatic volunteers were exposed for six hours to a single exposure of air and three exposures of the combination of 400 ppb NO2 + 200 ppb SO2 in randomised order, and then challenged with increasing concentrations of Dermatophagoides pteronyssinus allergen either immediately after exposure to air, or immediately, 24 hours or 48 hours after exposure to the combination of the two pollutants, until a 20% fall in forced expiratory volume in one second (FEV1) was recorded. RESULTS: Exposure to 400 ppb NO2 + 200 ppb SO2 significantly decreased the dose of D pteronyssinus allergen required to produce a 20% fall in FEV1 (PD20FEV1) at all times after exposure when compared with air. The mean percentage changes in allergen PD20FEV1 immediately, 24 hours, and 48 hours after exposure to 400 ppb NO2 + 200 ppb SO2 were -37% (95% confidence intervals (CI) -50 to -23), -63% (CI -75 to -51), and -49% (CI -75 to -28.8), respectively, when compared with the PD20FEV1 after air exposure and were significant at all time points studied. The allergen PD20FEV1 at 24 hours after exposure to the combination of the two pollutants was also found to be significantly lower when compared with that immediately after exposure to the two pollutants. CONCLUSION: These results demonstrate that exposure to a combination of NO2 and SO2, at concentrations which can be encountered during episodes of increased outdoor and indoor air pollution, enhances the airway response to inhaled allergen in asthmatic subjects. This effect persists over a period of 24-48 hours and is maximal 24 hours after exposure to these air pollutants.

Adult↗
PubMed2002

Total microbial activity and microbial composition of a mangrove sediment are reduced by oil pollution at a site in the Arabian Gulf.

In a study carried out to determine the effect of oil pollution on the microbiota of sediment associated with mangroves in the United Arab Emirates, sediment samples were collected from oil-polluted and nonpolluted mangrove sites. The levels of the total recoverable hydrocarbons and the polycyclic aromatic hydrocarbons assayed were noticeably higher in the polluted sediment. Microbial activity as measured by the hydrolysis of fluorescein diacetate and by the total populations of the culturable aerobic and anaerobic bacteria, streptomycete and non-streptomycete actinomycetes, and filamentous fungi and yeasts was significantly (P < 0.05) lower in the polluted than in the nonpolluted sediment. The estimated total aerobic and anaerobic hydrocarbon-utilizing bacteria were significantly (P < 0.05) higher in the polluted than in the nonpolluted sediments. Four days after the addition of the water-soluble fractions of the light Arabian crude oil to the nonpolluted sediment, at 10 different concentrations, there was a significant (P < 0.05) reduction (65%) in the microbial activity of the sediment compared with that of nonamended sediment. Concentrations of water-soluble fractions at 0.1% and above significantly and progressively reduced microbial activity, with total cessation of activity recorded at levels >50%. This study is the first to evaluate the effect of oil pollution on aerobic and anaerobic microbial flora of sediment of mangrove communities.

Arabia↗
PubMed2006

Environmental cardiology: studying mechanistic links between pollution and heart disease.

Environmental factors are considered key determinants of cardiovascular disease. Although lifestyle choices such as smoking, diet, and exercise are viewed as major environmental influences, the contribution of pollutants and environmental chemicals is less clear. Accumulating evidence suggests that exposure to pollutants and chemicals could elevate the risk of cardiovascular disease. Many epidemiological studies report that exposure to fine particles present in ambient air is associated with an increase in cardiovascular mortality. Statistically significant relationships between particulate air pollution and ischemic heart disease, arrhythmias, and heart failure have been reported. Animal studies show that exposure to ambient air particles increases peripheral thrombosis and atherosclerotic lesion formation. Exposures to arsenic, lead, cadmium, pollutant gases, solvents, and pesticides have also been linked to increased incidence of cardiovascular disease. Mechanistically, these effects have been attributed to changes in the synthesis or reactivity of nitric oxide that may be caused by environmental oxidants or increased endogenous production of reactive oxygen species. Additional studies are urgently needed to: identify the contribution of individual pollutants to specific aspects of cardiovascular disease; establish causality; elucidate the underlying physiological and molecular mechanisms; estimate the relative susceptibility of diseased and healthy individuals and that of specific population groups; and determine whether pollutant exposure are risk correlates, that is, whether they influence major risk factors, such as hypertension, cholesterol, or diabetes, or whether they contribute to the absolute risk of heart disease. Collectively, these investigations could contribute to the emergent field of environmental cardiology.

Air Pollution↗
PubMed2003

Evidence for an association between air pollution and daily stroke admissions in Kaohsiung, Taiwan.

BACKGROUND AND PURPOSE: Many studies have reported increases in daily cardiovascular mortality and hospital admissions associated with increases in levels of air pollutants. However, little is known about the relationship between hospital admissions for stroke and air pollution. This study was undertaken to determine whether there is an association between air pollution and hospital admissions for stroke in Kaohsiung, Taiwan. METHODS: Data on a total of 23 179 stroke admissions were obtained for the period 1997 through 2000. The relative risk of hospital admissions was estimated with a case-crossover approach. RESULTS: In the single-pollutant models, on warm days (> or =20 degrees C), significant positive associations were found between levels of PM10, NO2, SO2, CO, and O3 and both primary intracerebral hemorrhage and ischemic stroke admissions. On cool days (<20 degrees C), only CO levels and ischemic stroke admissions were significantly associated. For the 2-pollutant models, PM10 and NO2 remained consistently and significantly associated with admissions for both types of stroke on warm days. We observed estimated relative risks of 1.54 (95% confidence interval [95%], 1.31 to 1.81) and 1.56 (95% CI, 1.32 to 1.84) for primary intracerebral hemorrhage for each interquartile range increase in PM10 and NO2. The values for ischemic stroke were 1.46 (95% CI, 1.32 to 1.61) and 1.55 (95% CI, 1.40 to 1.71), respectively. The effects of CO, SO2, and O3 were mostly nonsignificant when either NO2 or PM10 was controlled for. CONCLUSIONS: This study provides an association between exposure to air pollution and hospital admissions for stroke.

Air Pollution↗
PubMed1999

Human isolated airway contraction: interaction between air pollutants and passive sensitization.

Although there is epidemiological evidence that an increase in allergic diseases such as asthma may be linked to air pollution, there is little experimental data to address this issue. The aim of this study was thus to investigate the interaction between passive sensitization and exposure to pollutants in human isolated airways. We have examined (1) the effect of a preexposure to pollutants on the contraction of sensitized bronchi to a specific antigen, and (2) the effect of passive sensitization on the contraction to nonspecific agonists in bronchi preexposed to pollutants. In tissues sensitized by incubation in sera from asthmatic patients, preexposure to 0.3 microM acrolein (an aldehyde) for 10 min or 20 min significantly increased the maximal contractile response to the antigen Dermatophagoides pteronyssinus (D. pter.) by 20.5 +/- 6.5 and 34.9 +/- 7.4%, respectively. Similarly, preexposure to ozone (1 ppm for 20 min) increased the response to D. pter. by 25.3 +/- 11.3%. On the other hand, passive sensitization increased the contractile response to carbachol or histamine of bronchial rings preexposed to 0.3 microM acrolein for 10 min by 33.5 +/- 6.2% and 32.5 +/- 5.1%, respectively. This study provides a proof of principle in vitro for a combined effect of immunological sensitization and exposure to pollutants, i.e., passive sensitization and exposure to pollutants act in a synergistic manner on human bronchial smooth muscle reactivity in response to both specific antigen and nonspecific agonists.

Acrolein↗
PubMed2004

Traffic-related air pollution near busy roads: the East Bay Children's Respiratory Health Study.

Recent studies, primarily in Europe, have reported associations between respiratory symptoms and residential proximity to traffic; however, few have measured traffic pollutants or provided information about local air quality. We conducted a school-based, cross-sectional study in the San Francisco Bay Area in 2001. Information on current bronchitis symptoms and asthma, home environment, and demographics was obtained by parental questionnaire (n = 1,109). Concentrations of traffic pollutants (particulate matter, black carbon, total nitrogen oxides [NO(X)], and nitrogen dioxide [NO(2)]) were measured at 10 school sites during several seasons. Although pollutant concentrations were relatively low, we observed differences in concentrations between schools nearby versus those more distant (or upwind) from major roads. Using a two-stage multiple-logistic regression model, we found associations between respiratory symptoms and traffic-related pollutants. Among those living at their current residence for at least 1 year, the adjusted odds ratio for asthma in relationship to an interquartile difference in NO(X) was 1.07 (95% confidence interval, 1.00-1.14). Thus, we found spatial variability in traffic pollutants and associated differences in respiratory symptoms in a region with good air quality. Our findings support the hypothesis that traffic-related pollution is associated with respiratory symptoms in children.

Air Pollutants↗
PubMed2005

Air pollution and markers of inflammation and coagulation in patients with coronary heart disease.

RATIONALE: Ambient air pollution has been shown to be associated with cardiovascular morbidity and mortality. OBJECTIVES: A prospective panel study was conducted to study the early physiologic reactions characterized by blood biomarkers of inflammation, endothelial dysfunction, and coagulation in response to daily changes in air pollution in Erfurt, Germany. METHODS: Blood parameters were repeatedly measured in 57 male patients with coronary heart disease during the winter of 2000/2001. Fixed-effects linear and logistic regression models were applied, adjusting for trend, weekday, and meteorologic parameters. MEASUREMENTS: Hourly data on ultrafine particles (UFPs; number concentration of particles from 0.01 to 0.1 microm), mass concentration of particles less than 10 (PM(10)) and 2.5 microm in diameter, elemental and organic carbon, gaseous pollutants, and meteorologic data were collected at central monitoring sites. MAIN RESULTS: Increased levels of C-reactive protein above the 90th percentile were observed for an increase in air pollution concentrations of one interquartile range. The effect was strongest for accumulation mode particles, with a delay of 2 d (odds ratio [OR], 3.2; confidence interval [CI], 1.7, 6.0). Results were consistent for UFPs and PM(10), which also showed a 2-d delayed response (OR, 2.3; CI, 1.3, 3.8; and OR, 2.2; CI, 1.2, 3.8, respectively). However, not all of the blood markers of endothelial dysfunction and coagulation increased consistently in association with air pollutants. CONCLUSION: These results suggest that inflammation as well as parts of the coagulation pathway may contribute to the association between particulate air pollution and coronary events.

Aged↗
PubMedDate not supplied

Metal storage and transport proteins increase after exposure of the rat lung to an air pollution particle.

With the single exception of mercury, all metals in the atmosphere are associated with particles. The lungs are subsequently exposed to metals present in air pollution particles on a continuous basis. Because metal exposure can be associated with an oxidative stress, a mechanism that isolates the metal in a chemically less reactive form would be of benefit. We tested the hypothesis that the concentrations of both lactoferrin and ferritin in the rat lung increase after exposure to a metal-rich emission source air pollution particle. Using immunohistochemistry, we characterized changes in the concentrations of ferritin and lactoferrin after exposure of rats to an emission source air pollution particle. Lavage metal concentrations, measured by inductively coupled plasma emission spectroscopy, increased 4 hr after exposure to an oil fly ash. After exposure to this metal-rich emission source air pollution particle, ferritin concentrations in the lower respiratory tract increased. Comparable to the iron-storage protein, concentrations of both lactoferrin and transferrin were elevated after exposure. The greatest concentrations of ferritin, lactoferrin, and transferrin occurred at approximately 24 hr after exposure to the air pollution particle. Levels then decreased, and by 96 hr after instillation of the oil fly ash, ferritin, lactoferrin, and transferrin were not elevated relative to those animals exposed to saline. We conclude that, in response to an emission source air pollution particle with high concentrations of metals, there is an increase in ferritin, lactoferrin, and transferrin concentrations in the lungs of the host. The function of these increases in iron-binding proteins may be to control the oxidative stress associated with the exposure to metals.

Air Pollution↗
PubMedDate not supplied

Meta-analysis of the Italian studies of short-term effects of air pollution (MISA), 1990-1999.

A meta-analysis of short-term effects of air pollution on health in eight Italian cities from 1990 to 1999 is presented. Death certificates and hospital admission data as well as daily concentrations of pollutants were collected. The same generalized linear model adjusted for age, day of the week, holidays, influenza epidemics, meteorological variables, and seasonality pattern was fitted to the city data. City-specific model selection was not done. In the meta-analysis, for each outcome, the city-specific estimates for each pollutant were combined using fixed and random-effects models. Hierarchical Bayesian models were use to investigate the effects of PM10 in detail. Each pollutant (SO2, NO2, CO, PM10, O3) was significantly associated with mortality for natural causes. The effect of PM10 on mortality was greater during the warm season and for elderly. A north-south gradient in risk was observed for total natural mortality. The excess risks on hospital admission were modified by deprivation score and by the NO2/PM10 ratio. Results add evidence for an association between air pollution and early mortality or morbidity and support the hypothesis of a synergism between meteorological variables and air pollution.

Adolescent↗
PubMed1996

Epidemiological studies of the respiratory effects of air pollution.

Environmental epidemiological studies of the health effects of air pollution have been major contributors to the understanding of such effects. The chronic effects of atmospheric pollutants have been studied, but, except for the known respiratory effects of particulate matter (PM), they have not been studied conclusively. There are ongoing studies of the chronic effects of certain pollutant classes, such as ozone, acid rain, airborne toxics, and the chemical form of PM (including diesel exhaust). Acute effects on humans due to outdoor and indoor exposures to several gases/fumes and PM have been demonstrated in epidemiological studies. However, the effects of these environmental factors on susceptible individuals are not known conclusively. These acute effects are especially important because they increase the human burden of minor illnesses, increase disability, and are thought to decrease productivity. They may be related to the increased likelihood of chronic disease as well. Further research is needed in this latter area, to determine the contributions of the time-related activities of individuals in different microenvironments (outdoors, in homes, in transit). Key elements of further studies are the assessment of total exposure to the different pollutants (occurring from indoor and outdoor source) and the interactive effects of pollutants. Major research areas include determination of the contributions of indoor sources and of vehicle emissions to total exposure, how to measure such exposures, and how to measure human susceptibility and responses (including those at the cellular and molecular level). Biomarkers of exposures, doses and responses, including immunochemicals, biochemicals and deoxyribonucleic acid (DNA) adducts, are beginning to promote some basic knowledge of exposure-response, especially the mechanisms. These will be extremely useful additions to standard physiological, immunological, and clinical instruments, and the understanding of biological plausibility. The outcomes of all this work will be the management of risks and the prevention of respiratory diseases related to air pollution.

Air Pollutants↗
PubMed1996

Asthmatic bronchial hyperresponsiveness varies with ambient levels of summertime air pollution.

It is widely believed that the mechanisms of action of outdoor air pollutants are the same as those found in the laboratory, although few studies have attempted to clarify this issue. This study investigates the relationship of asthmatic bronchial hyperresponsiveness (BHR), a marker of airway inflammation, and pulmonary function to ambient levels of summertime air pollution. Thirty eight nonsmoking adult asthmatic subjects underwent repeated measurement of methacholine BHR, using Yan's method, at differing levels of air pollution (O3, SO2, NO2, smoke) during summer 1993. A total of 109 evaluable tests were performed: 31 subjects completed three or more challenge tests, and seven managed two. Levels of all pollutants remained within current World Health Organization (WHO) Guidelines for Health. Changes in BHR were found to correlate significantly with changes in the levels of 24 h mean SO2, NO2 and smoke; 48 h mean NO2 and smoke; 24 h lag NO2; although the effect was only small, accounting for approximately 10% of the variability in within-subject BHR between visits. Twenty four hour lag NO2 was also associated with forced vital capacity (FVC). In conclusion, in subjects with asthma, methacholine bronchial hyperresponsiveness varies with ambient levels of summertime air pollution. This suggests that changes in airway inflammation underlie the increased respiratory morbidity known to accompany pollution episodes.

Adolescent↗
PubMed1997

Air pollution and daily admissions for chronic obstructive pulmonary disease in 6 European cities: results from the APHEA project.

We investigated the short-term effects of air pollution on hospital admissions for chronic obstructive pulmonary disease (COPD) in Europe. As part of a European project (Air Pollution and Health, a European Approach (APHEA)), we analysed data from the cities of Amsterdam, Barcelona, London, Milan, Paris and Rotterdam, using a standardized approach to data eligibility and statistical analysis. Relative risks for daily COPD admissions were obtained using Poisson regression, controlling for: seasonal and other cycles; influenza epidemics; day of the week; temperature; humidity and autocorrelation. Summary effects for each pollutant were estimated as the mean of each city's regression coefficients weighted by the inverse of the variance, allowing for additional between-cities variance, as necessary. For all ages, the relative risks (95% confidence limits (95% CL)) for a 50 microg x m(-3) increase in daily mean level of pollutant (lagged 1-3 days) were (95% CL): sulphur dioxide 1.02 (0.98, 1.06); black smoke 1.04 (1.01, 1.06); total suspended particulates 1.02 (1.00, 1.05), nitrogen dioxide 1.02 (1.00, 1.05) and ozone (8 h) 1.04 (1.02, 1.07). The results confirm that air pollution is associated with daily admissions for chronic obstructive pulmonary disease in European cities with widely varying climates. The results for particles and ozone are broadly consistent with those from North America, though the coefficients for particles are substantially smaller. Overall, the evidence points to a causal relationship but the mechanisms of action, exposure response relationships and pollutant interactions remain unclear.

Air Pollution↗
PubMed2000

Effects of ambient air pollution on symptoms of asthma in Seattle-area children enrolled in the CAMP study.

We observed a panel of 133 children (5-13 years of age) with asthma residing in the greater Seattle, Washington, area for an average of 58 days (range 28-112 days) during screening for enrollment in the Childhood Asthma Management Program (CAMP) study. Daily self-reports of asthma symptoms were obtained from study diaries and compared with ambient air pollution levels in marginal repeated measures logistic regression models. We defined days with asthma symptoms as any day a child reported at least one mild asthma episode. All analyses were controlled for subject-specific variables [age, race, sex, baseline height, and FEV(1) PC(20) concentration (methacholine provocative concentration required to produce a 20% decrease in forced expiratory volume in 1 sec)] and potential time-dependent confounders (day of week, season, and temperature). Because of variable observation periods for participants, we estimated both between- and within-subject air pollutant effects. Our primary interest was in the within-subject effects: the effect of air pollutant excursions from typical levels in each child's observation period on the odds of asthma symptoms. In single-pollutant models, the population average estimates indicated a 30% [95% confidence interval (CI), 11-52%] increase for a 1-ppm increment in carbon monoxide lagged 1 day, an 18% (95% CI, 5-33%) increase for a 10-microg/m(3) increment in same-day particulate matter < 1.0 microm (PM(1.0)), and an 11% (95% CI, 3-20%) increase for a 10-microg/m(3) increment in particulate matter < 10 microm (PM(10)) lagged 1 day. Conditional on the previous day's asthma symptoms, we estimated 25% (95% CI, 10-42%), 14% (95% CI, 4-26%), and 10% (95% CI, 3-16%) increases in the odds of asthma symptoms associated with increases in CO, PM(1.0), and PM(10), respectively. We did not find any association between sulfur dioxide (SO(2)) and the odds of asthma symptoms. In multipollutant models, the separate pollutant effects were smaller. The overall effect of an increase in both CO and PM(1. 0) was a 31% (95% CI, 11-55%) increase in the odds of symptoms of asthma. We conclude that there is an association between change in short-term air pollution levels, as indexed by PM and CO, and the occurrence of asthma symptoms among children in Seattle. Although PM effects on asthma have been found in other studies, it is likely that CO is a marker for vehicle exhaust and other combustion by-products that aggravate asthma.

Adolescent↗
PubMed2001

Air quality in postunification Erfurt, East Germany: associating changes in pollutant concentrations with changes in emissions.

The unification of East and West Germany in 1990 resulted in sharp decreases in emissions of major air pollutants. This change in air quality has provided an opportunity for a natural experiment to evaluate the health impacts of air pollution. We evaluated airborne particle size distribution and gaseous co-pollutant data collected in Erfurt, Germany, throughout the 1990s and assessed the extent to which the observed changes are associated with changes in the two major emission sources: coal burning for power production and residential heating, and motor vehicles. Continuous data for sulfur dioxide, total suspended particulates (TSP), nitric oxide, carbon monoxide, and meteorologic parameters were available for 1990-1999, and size-selective particle number and mass concentration measurements were made during winters of 1991 and 1998. We used hourly profiles of pollutants and linear regression analyses, stratified by year, weekday/weekend, and hour, using NO and SO(2) as markers of traffic- and heating-related combustion sources, respectively, to study the patterns of various particle size fractions. Supplementary data on traffic and heating-related sources were gathered to support hypotheses linking these sources with observed changes in ambient air pollution levels. Substantially decreased (19-91%) concentrations were observed for all pollutants, with the exception of particles in the 0.01-0.03 microm size range (representing the smallest ultrafine particles that were measured). The number concentration for these particles increased by 115% between 1991 and 1998. The ratio of these ultrafine particles to TSP also increased by more than 500%, indicating a dramatic change in the size distribution of airborne particles. Analysis of hourly concentration patterns indicated that in 1991, concentrations of SO(2) and larger particle sizes were related to residential heating with coal. These peaks were no longer evident in 1998 due to decreases in coal consumption and consequent decreased emissions of SO(2) and larger particles. These decreases in coal combustion and the decreased concentrations of SO(2) and particles of larger size classes may have led to decreased particle scavenging and may be partially responsible for the observed increases in ultrafine particles. Traffic-related changes, such as increased numbers of trucks and increased use of diesel vehicles in Erfurt, were also associated with increased number concentrations of ultrafine particles. Morning particle peaks of all sizes were associated with NO and CO (markers for traffic) in both the 1991 and 1998 periods. There were significant differences in the ultrafine particle levels for morning hours between 1991 and 1998, suggesting that traffic was the cause of this increase.

Air Pollutants↗
PubMed2001

Air pollution and blood markers of cardiovascular risk.

Recent studies have linked air pollution to tens of thousands of premature cardiovascular deaths per year. The mechanisms of such associations remain unclear. In this study we examine the association between blood markers of cardiovascular risk and air pollution in a national sample of the U.S. population. Air pollution concentrations were merged to subjects in the Third National Health and Nutrition Examination Survey (NHANES III) in the United States, and the association with fibrinogen levels and counts of platelets and white blood cells were examined. The subjects in NHANES III are a representative sample of the U.S. population. Regressions controlled for age, race, sex, body mass index, current smoking, and number of cigarettes per day. The complex survey design was dealt with using mixed models with a random sampling site effect. In single-pollutant models, PM(10) (particulate matter with a mass median aerodynamic diameter less than 10 microm) was associated with all three outcomes (p< 0.05): Sulfur dioxide (SO(2)) was significantly associated only with white cell counts, nitrogen dioxide (NO(2)) with platelet counts and fibrinogen, and ozone with none of the outcomes. In two-pollutant models, PM(10) remained a significant predictor of white cell counts controlling for SO(2) but not vice versa. PM(10) was marginally significant in a model for platelet counts with NO(2), and the sign of the NO(2) coefficient was reversed. These results were stable with control for indoor exposures (wood stoves, environmental tobacco smoke, gas stoves, fireplaces), dietary risk factors (saturated fat, alcohol, caffeine intake, n-3 fatty acids), and serum cholesterol. The magnitude of the effects are modest [e.g., 13 microg/dL fibrinogen for an interquartile range (IQR) change in PM(subscript)10(/subscript), 95% confidence interval (CI) 4.6-22.1 mg/dL]. However, the odds ratio of being in the top 10% of fibrinogen for the same IQR change was 1.77 (95% CI 1.26-2.49). These effects provide considerable biologic plausibility to the mortality studies. PM(10), but not gaseous air pollutants, is associated with blood markers of cardiovascular risk, and this may explain epidemiologic associations with early deaths.

Adult↗
PubMed2000

Epidemiology of fine particulate air pollution and human health: biologic mechanisms and who's at risk?

This article briefly summarizes the epidemiology of the health effects of fine particulate air pollution, provides an early, somewhat speculative, discussion of the contribution of epidemiology to evaluating biologic mechanisms, and evaluates who's at risk or is susceptible to adverse health effects. Based on preliminary epidemiologic evidence, it is speculated that a systemic response to fine particle-induced pulmonary inflammation, including cytokine release and altered cardiac autonomic function, may be part of the pathophysiologic mechanisms or pathways linking particulate pollution with cardiopulmonary disease. The elderly, infants, and persons with chronic cardiopulmonary disease, influenza, or asthma are most susceptible to mortality and serious morbidity effects from short-term acutely elevated exposures. Others are susceptible to less serious health effects such as transient increases in respiratory symptoms, decreased lung function, or other physiologic changes. Chronic exposure studies suggest relatively broad susceptibility to cumulative effects of long-term repeated exposure to fine particulate pollution, resulting in substantive estimates of population average loss of life expectancy in highly polluted environments. Additional knowledge is needed about the specific pollutants or mix of pollutants responsible for the adverse health effects and the biologic mechanisms involved.

Air Pollution↗
PubMed2004

Is the association of airborne particles with daily deaths confounded by gaseous air pollutants? An approach to control by matching.

Although particulate air pollution has been associated with increased numbers of daily deaths in dozens of cities around the world, issues still remain about the association. Some have questioned the complex modeling used to control for season in Poisson regression or the role of gaseous air pollutants as potential confounders of the association. I examined the association between deaths and particulate matter with an aerodynamic diameter less than or equal to 10 microm (PM10) using a case-crossover design. In this approach, the pollution on the day of each death is contrasted with the pollution level on control days when the subject did not die. Season and gaseous air pollutants were controlled by matching. Control days were chosen within the same month of the same year to control for season, and matched on either sulfur dioxide (SO2; within 1 ppb), nitrogen dioxide (within 1 ppb), maximum ozone (within 2 ppb), or carbon monoxide (within 0.03 ppm). The analysis was conducted in 14 U.S. cities that have daily PM10 monitoring. After matching, there were about 400,000 deaths in each analysis. Results were combined across cities using a maximum likelihood method. PM10 was a significant predictor of mortality when controlling for gaseous air pollutants, with effect sizes ranging from a 0.45% increase per 10 microg/m3 increment of PM10 [95% confidence interval (CI), 0.12-0.79%] when matched on maximum hourly ozone levels, to a 0.81% increase per 10 microg/m3 increment of PM10 (95% CI, 0.47-1.16%) when matched on 24-hr average SO2.

Air Pollution↗
PubMed2004

Does particulate air pollution contribute to infant death? A systematic review.

There is now substantial evidence that both short- and long-term increases in ambient air pollution are associated with increased mortality and morbidity in adults and children. Children's health is particularly vulnerable to environmental pollution, and infant mortality is still a major contributor to childhood mortality. In this systematic review we summarize and evaluate the current level of epidemiologic evidence of an association between particulate air pollution and infant mortality. We identified relevant publications using database searches with a comprehensive list of search terms and other established search methods. We included articles in the review according to specified inclusion criteria. Fifteen studies met our inclusion criteria. Evidence of an association between particulate air pollution and infant mortality in general was inconsistent, being reported from locations with largely comparable pollution levels. There was some evidence that the strength of association with particulate matter differed by subgroups of infant mortality. It was more consistent for postneonatal mortality due to respiratory causes and sudden infant death syndrome. Differential findings for various mortality subgroups within studies suggest a stronger association of particulate air pollution with some causes of infant death. Research is needed to confirm and clarify these links, using the most appropriate methodologies for exposure assessment and control of confounders.

Air Pollutants↗