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PubMed2006

Acute symptoms related to air pollution in urban areas: a study protocol.

BACKGROUND: The harmful effects of urban air pollution on general population in terms of annoying symptoms are not adequately evaluated. This is in contrast to the hospital admissions and short term mortality. The present study protocol is designed to assess the association between the level of exposure to certain ambient air pollutants and a wide range of relevant symptoms. Awareness of the impact of pollution on the population at large will make our estimates of the pertinent covert burden imposed on the society more accurate. METHODS/DESIGN: A cross sectional study with spatial analysis for the addresses of the participants was conducted. Data were collected via telephone interviews administered to a representative sample of civilians over age four in the city. Households were selected using random digit dialling procedures and randomization within each household was also performed to select the person to be interviewed. Levels of exposure are quantified by extrapolating the addresses of the study population over the air pollution matrix of the city at the time of the interview and also for different lag times. This information system uses the data from multiple air pollution monitoring stations in conjunction with meteorological data. General linear models are applied for statistical analysis. DISCUSSION: The important limitations of cross-sectional studies on acute effects of air pollution are personal confounders and measurement error for exposure. A wide range of confounders in this study are controlled for in the statistical analysis. Exposure error may be minimised by employing a validated geographical information system that provides accurate estimates and getting detailed information on locations of individual participants during the day. The widespread operation of open air conditioning systems in the target urban area which brings about excellent mixing of the outdoor and indoor air increases the validity of outdoor pollutants levels that are taken as exposure levels.

Air Pollution↗
PubMed2006

The association between low level exposures to ambient air pollution and term low birth weight: a retrospective cohort study.

BACKGROUND: Studies in areas with relatively high levels of air pollution have found some positive associations between exposures to ambient levels of air pollution and several birth outcomes including low birth weight (LBW). The purpose of this study was to examine the association between LBW among term infants and ambient air pollution, by trimester of exposure, in a region of lower level exposures. METHODS: The relationship between LBW and ambient levels of particulate matter up to 10 um in diameter (PM10), sulfur dioxide (SO2) and ground-level ozone (O3) was evaluated using the Nova Scotia Atlee Perinatal Database and ambient air monitoring data from the Environment Canada National Air Pollution Surveillance Network and the Nova Scotia Department of Environment. The cohort consisted of live singleton births (> or =37 weeks of gestation) between January 1, 1988 and December 31, 2000. Maternal exposures to air pollution were assigned to women living within 25 km of a monitoring station at the time of birth. Air pollution was evaluated as a continuous and categorical variable (using quartile exposures) for each trimester and relative risks were estimated from logistic regression, adjusted for confounding variables. RESULTS: There were 74,284 women with a term, singleton birth during the study period and with exposure data. In the analyses unadjusted for year of birth, first trimester exposures in the highest quartile for SO2 and PM10 suggested an increased risk of delivering a LBW infant (relative risk = 1.36, 95% confidence interval = 1.04 to 1.78 for SO2 exposure and relative risk = 1.33, 95% confidence interval = 1.02 to 1.74 for PM10). After adjustment for birth year, the relative risks were attenuated somewhat and not statistically significant. A dose-response relationship for SO2 was noted with increasing levels of exposure. No statistically significant effects were noted for ozone. CONCLUSION: Our results suggest that exposure during the first trimester to relatively low levels of some air pollutants may be associated with a reduction in birth weight in term-born infants. These findings have implications for the development of effective risk management strategies to minimize the public health impacts for pregnant women.

Adult↗
PubMed1986

Implications of air pollution effects on athletic performance.

Both controlled human studies and observational studies suggest that air pollution adversely affects athletic performance during both training and competition. The air pollution dosage during exercise is much higher than during rest because of a higher ventilatory rate and both nasal and oral breathing in the former case. For example, sulfur dioxide, which is a highly water-soluble gas, is almost entirely absorbed in the upper respiratory tract during nasal breathing. However, with oral pharyngeal breathing, the amount of sulfur dioxide that is absorbed is significantly less, and with exercise and oral pharyngeal breathing a significant decrease in upper airway absorption occurs, resulting in a significantly larger dosage of this pollutant being delivered to the tracheobronchial tree. Recently, several controlled human studies have shown that the combination of exercise and pollutant exposure (SO2 or O3) caused a marked bronchoconstriction and reduced ventilatory flow when compared to pollution exposure at rest. In a situation like the Olympic Games where milliseconds and millimeters often determine the success of athletes, air pollution can be an important factor in affecting their performance. This paper examines possible impacts of air pollution on athletic competition.

Air Pollution↗
PubMed2000

Semen quality and reproductive health of young Czech men exposed to seasonal air pollution.

This study of male reproductive health in the Czech Republic resulted from community concern about potential adverse effects of air pollution. We compared young men (18 years of age) living in Teplice, a highly industrialized district with seasonally elevated levels of air pollution, to those from Prachatice, a rural district with relatively clean air. Surveys were scheduled for either late winter, after the season of higher air pollution, or at the end of summer, when pollution was low. Participation included a physical examination, donation of a semen sample, and completion of a questionnaire on health, personal habits, and exposure to solvents and metals through work or hobby. Analysis of data from 408 volunteers showed that the men from Teplice and Prachatice were similar in physical characteristics, personal habits, and work- or hobby-related exposures. Sixty-six percent (272) of these men donated a single semen sample for routine semen analysis, computer-aided sperm motion analysis, and sperm chromatin structure assay. The mean (median) sperm concentration and sperm count were 61. 2 (44.0) million/mL semen and 113.3 (81.5) million, respectively, and were not associated with district of residence or period of elevated air pollution. However, periods of elevated air pollution in Teplice were significantly associated with decrements in other semen measures including proportionately fewer motile sperm, proportionately fewer sperm with normal morphology or normal head shape, and proportionately more sperm with abnormal chromatin. These results suggest that young men may experience alterations in sperm quality after exposure to periods of elevated air pollution, without changes in sperm numbers.

Adolescent↗
PubMed2001

Gaseous pollutants in particulate matter epidemiology: confounders or surrogates?

Air pollution epidemiologic studies use ambient pollutant concentrations as surrogates of personal exposure. Strong correlations among numerous ambient pollutant concentrations, however, have made it difficult to determine the relative contribution of each pollutant to a given health outcome and have led to criticism that health effect estimates for particulate matter may be biased due to confounding. In the current study we used data collected from a multipollutant exposure study conducted in Baltimore, Maryland, during both the summer and winter to address the potential for confounding further. Twenty-four-hour personal exposures and corresponding ambient concentrations to fine particulate matter (PM(2.5)), ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide were measured for 56 subjects. Results from correlation and regression analyses showed that personal PM(2.5) and gaseous air pollutant exposures were generally not correlated, as only 9 of the 178 individual-specific pairwise correlations were significant. Similarly, ambient concentrations were not associated with their corresponding personal exposures for any of the pollutants, except for PM(2.5), which had significant associations during both seasons (p < 0.0001). Ambient gaseous concentrations were, however, strongly associated with personal PM(2.5) exposures. The strongest associations were shown between ambient O(3) and personal PM(2.5) (p < 0.0001 during both seasons). These results indicate that ambient PM(2.5) concentrations are suitable surrogates for personal PM(2.5) exposures and that ambient gaseous concentrations are surrogates, as opposed to confounders, of PM(2.5). These findings suggest that the use of multiple pollutant models in epidemiologic studies of PM(2.5) may not be suitable and that health effects attributed to the ambient gases may actually be a result of exposures to PM(2.5).

Adolescent↗
PubMed2001

Cardiovascular effects of air pollution: what to measure in ECG?

Epidemiologic evidence indicates that air pollution adversely affects the cardiovascular system, leading to increased cardiovascular morbidity and mortality. However, the mechanisms of such an association are unknown. Although potential mechanisms of deleterious effects of air pollution may involve response of the respiratory system, immunologic response, or coagulation abnormalities, the cardiovascular system seems to be the common end point of these pathways. Cardiovascular response to any stress (which may include air pollution) is a consequence of a complex interplay between the autonomic nervous system governing centrally mediated control of the cardiovascular system, a myocardial substrate (current state of the myocardium) altered in the course of disease processes, and myocardial vulnerability leading to arrhythmogenic or ischemic response. Through the use of standard electrocardiograms (ECGs), exercise ECG testing, and long-term ambulatory ECG monitoring, modern electrocardiology makes a valuable contribution to understanding the different mechanistic factors involved in the increase in adverse cardiovascular events due to air pollution. Heart rate variability analysis can provide quantitative insight into the autonomic response of the cardiovascular system to air pollution. Analysis of ventricular repolarization in an ECG (both duration and morphology) gives valuable information about the status and dynamic behavior of myocardium, reflecting myocardial substrate and vulnerability. ST-segment analysis of ECGs is used routinely to monitor the magnitude of ischemia and could be used to monitor subtle changes in the myocardium in subjects exposed to air pollution. Comprehensive analysis of ECG parameters describing the influence of the autonomic nervous system, the role of myocardial substrate, and the contribution of myocardial vulnerability could and should be employed in air pollution studies, especially as those mechanistic components have been proven to contribute to increased cardiovascular morbidity and mortality in general.

Air Pollutants↗
PubMed2002

Association of asthma symptoms with peak particulate air pollution and effect modification by anti-inflammatory medication use.

Maxima of hourly data from outdoor monitors may capture adverse effects of outdoor particulate matter (PM) exposures in asthmatic children better than do 24-hr PM averages, which form the basis of current regulations in the United States. Also, asthmatic children on anti-inflammatory medications may be protected against the proinflammatory effects of air pollutants and aeroallergens. We examined strengths of pollutant associations with asthma symptoms between subgroups of asthmatic children who were on versus not on regularly scheduled anti-inflammatory medications, and tested associations for different particle averaging times. This is a daily panel study of 22 asthmatic children (9-19 years of age) followed March through April 1996 (1,248 person-days). They lived in nonsmoking households in a semirural area of Southern California within the air inversion mixing zone (range, 1,200-2,100 feet) with transported air pollution from urban areas of Southern California. The dependent variable derived from diary ordinal scores is episodes of asthma symptoms that interfered with daily activities. Minimum to 90th-percentile levels of exposures at the outdoor monitoring site were 12-63 microg/m(3) for 1-hr PM < 10 microm in aerodynamic diameter (PM(10)); 8-46 microg/m(3) for 8-hr PM(10); 7-32 microg/m(3) for 24-hr PM(10); 45-88 ppb for 1-hr O(3); 6-26 ppb for 8-hr NO(2); 70-4,714 particles/m(3) for 12-hr daytime fungi; and 12-744 particles/m(3) for 24-hr pollen. Data were analyzed with generalized estimating equations controlling for autocorrelation. There was no confounding by weather, day of week, or linear time trend. Associations were notably stronger in 12 asthmatic children who were not taking anti-inflammatory medications versus 10 subjects who were. Odds ratios (95% confidence intervals) for asthma episodes in relation to lag 0 minimum to 90th-percentile pollutant changes were, respectively, 1-hr maximum PM(10), 1.92 (1.22-3.02) versus 0.96 (0.25-3.69); 8-hr maximum PM(10), 1.68 (0.91-3.09) versus 0.75 (0.18-3.04); 24-hr average PM(10), 1.35 (0.82-2.22) versus 0.80 (0.24-2.69); 1-hr maximum O(3), 1.28 (0.75-2.17) versus 0.76 (0.24-2.44); 8-hr maximum NO(2), 1.91 (1.07-3.39) versus 1.08 (0.30-3.93); 12-hr fungi, 1.89 (1.24-2.89) versus 0.90 (0.35-2.30); 24-hr pollen, 1.90 (0.99-3.67) versus 0.85 (0.18-3.91). Pollutant associations were stronger during respiratory infections in subjects not on anti-inflammatory medications. Although lag 0 1-hr maximum PM(10) showed the strongest association, the most robust associations were for lag 0 and 3-day moving averages (lags 0-2) of 8-hr maximum and 24-hr mean PM(10) in sensitivity analyses testing for thresholds. Most pollutant effects were largely driven by concentrations in the upper quintile. The divergence of exposure-response relationships by anti-inflammatory medication use is consistent with experimental data on inflammatory mechanisms of airborne pollutants and allergens.

Activities of Daily Living↗
PubMed2002

A tale of two cities: effects of air pollution on hospital admissions in Hong Kong and London compared.

The causal interpretation of reported associations between daily air pollution and daily admissions requires consideration of residual confounding, correlation between pollutants, and effect modification. If results obtained in Hong Kong and London--which differ in climate, lifestyle, and many other respects--were similar, a causal association would be supported. We used identical statistical methods for the analysis in each city. Associations between daily admissions and pollutant levels were estimated using Poisson regression. Nonparametric smoothing methods were used to model seasonality and the nonlinear dependence of admissions on temperature, humidity, and influenza admissions. For respiratory admissions (> or = 65 years of age), significant positive associations were observed with particulate matter < 10 microm in aerodynamic diameter (PM(10), nitrogen dioxide, sulfur dioxide, and ozone in both cities. These associations tended to be stronger at shorter lags in Hong Kong and at longer lags in London. Associations were stronger in the cool season in Hong Kong and in the warm season in London, periods during which levels of humidity are at their lowest in each city. For cardiac admissions (all ages) in both cities, significant positive associations were observed for PM(10), NO(2), and SO(2) with similar lag patterns. Associations tended to be stronger in the cool season. The associations with NO(2) and SO(2) were the most robust in two-pollutant models. Patterns of association for pollutants with ischemic heart disease were similar in the two cities. The associations between O(3) and cardiac admissions were negative in London but positive in Hong Kong. We conclude that air pollution has remarkably similar associations with daily cardiorespiratory admissions in both cities, in spite of considerable differences between cities in social, lifestyle, and environmental factors. The results strengthen the argument that air pollution causes detrimental short-term health effects.

Adolescent↗
PubMed2000

Winds of change: reducing transboundary air pollutants.

Sulfur dioxide, nitrogen oxides, volatile organic compounds, persistent organic pollutants, particulate matter, and heavy metals---air pollutants once thought to be problems that could be solved locally, where the effects occur---are all currently being discussed in international forums. A spate of meetings and agreements in recent months has shown many international governments to be more willing than ever to try to limit the amount of their air pollution that drifts into other countries. Prompting this policy shift are increasing emissions in some parts of the world, better monitoring, and an improved understanding of air pollution transport and the effects of air pollution. In most regions of the world, however, no international agreements on air pollution exist at all, while in others, many overlapping local, multilateral, and global agreements address the problem simultaneously. According to the World Health Organization, air pollution causes nearly 3 million deaths per year, and the U.S. Environmental Protection Agency estimates that ground-level ozone causes damage to U.S. crops totaling $1-2 billion each year.

Air Pollution↗
PubMed2001

Air pollution and child mortality: a time-series study in São Paulo, Brazil.

Although most available evidence relating air pollution and mortality was obtained for adults, pollution has been also associated with increased mortality in children, but in a significantly smaller number of studies. This study was designed to evaluate the association between child mortality and air pollution in the city of São Paulo, Brazil, from 1994 to 1997. Daily records of mortality due to respiratory diseases for children under 5 years of age were obtained from the municipal mortality information improvement program. Daily concentrations of sulfur dioxide (SO(2)), carbon monoxide (CO), inhalable particulate matter less than 10 microm in diameter (PM(10)), and ozone were obtained from the state air pollution controlling agency. Information on minimum daily temperature and on relative humidity were obtained from the Institute of Astronomy and Geophysics of the University of São Paulo. Statistical analysis was performed through generalized additive models considering a Poisson response distribution and a log link. Explanatory variables were time, temperature, humidity, and pollutant concentrations. The loess smoother was applied to time (in order to model seasonality) and temperature. Significant associations between mortality and concentrations of CO, SO(2), and PM(10) were detected. The coefficients (and standard errors) of these three pollutants were 0.0306 (0.0076), 0.0055 (0.0016), and 0.0014 (0.0006), respectively. The observed associations were dose dependent and quite evident after a short period of exposure (2 days). According to the proposed model and considering the mean of the pollutant concentration during the period of the study, the estimated proportions of respiratory deaths attributed to CO, SO(2), and PM(10), when considered individually, are around 15, 13, and 7%, respectively.

Air Pollution↗
PubMed2004

Cause-specific mortality and the extended effects of particulate pollution and temperature exposure.

Air pollution exposure studies in the past decade have focused on acute (days) or long-term (years) effects. We present an analysis of medium-term (weeks to months) exposure effects of particulate pollution and temperature. We assessed the associations of particulate pollution (black smoke) and temperature with age-standardized daily mortality rates over 17 years in Dublin, Ireland, using a polynomial distributed lag model of both temperature and particulate air pollution simultaneously through 40 days after exposure. When only acute effects (3-day mean) were considered, we found total mortality increased by 0.4% for each 10-microg/m3 increase in black smoke concentration. When deaths in the 40 days after exposure were considered, we found a 1.1% increase. For respiratory mortality, the estimated effect was 0.9% for acute exposures, but 3.6% for the extended follow-up. We found each increase in current-day temperature by 1 degree C was associated with a 0.4% increase in total mortality, whereas each decrease of 1 degree C was associated with a 2.6% increase in mortality in the following 40 days. For both temperature and pollution, the largest effects on cardiovascular mortality were observed immediately, whereas respiratory mortality was delayed and distributed over several weeks. These effects were two to three times greater than the acute effects reported in other studies, and approach the effects reported in longer-term survival studies. This analysis suggests that studies on the acute effects of air pollution have underestimated the total effects of temperature and particulate air pollution on mortality.

Adolescent↗
PubMed2004

Estimating the independent effects of multiple pollutants in the presence of measurement error: an application of a measurement-error-resistant technique.

Misclassification of exposure usually leads to biased estimates of exposure-response associations. This is particularly an issue in cases with multiple correlated exposures, where the direction of bias is uncertain. It is necessary to address this problem when considering associations with important public health implications such as the one between mortality and air pollution, because biased exposure effects can result in biased risk assessments. The National Morbidity and Mortality Air Pollution Study (NMMAPS) recently reported results from an assessment of multiple pollutants and daily mortality in 90 U.S. cities. That study assessed the independent associations of the selected pollutants with daily mortality in two-pollutant models. Excess mortality was associated with particulate matter of aerodynamic diameter less than or equal to 10 microm/m3 (PM10), but not with other pollutants, in these two pollutant models. The extent of bias due to measurement error in these reported results is unclear. Schwartz and Coull recently proposed a method that deals with multiple exposures and, under certain conditions, is resistant to measurement error. We applied this method to reanalyze the data from NMMAPS. For PM10, we found results similar to those reported previously from NMMAPS (0.24% increase in deaths per 10-microg/m3) increase in PM10). In addition, we report an important effect of carbon monoxide that had not been observed previously.

Air Pollutants↗
PubMed1980

Interaction between environmental pollutants and respiratory infections.

The major aspects that must be considered in studies of the health effects of environmental pollutants are: the direct damage due to the exposure, the role of pre-existing disease, and effects of the exposure on the response to secondary stresses. In experimental studies at concentrations of air pollutants found in urban environments frank toxicological responses are rarely observed. However, exposure to a secondary stress, i.e. respiratory challenge with infectious bacteria, can exacerbate the response of the experimental host. Changes in the resistance to respiratory infections provide a highly sensitive experimental animal model system, which is increasingly used in studies of health effects of air pollutants. This model indicates the impairment of the basic defense mechanisms of the respiratory system by the combined exposure to low concentrations of pollutants and the superimposed bacterial infection. Changes in the resistance to respiratory infections were studied in various species of laboratory animals. S. pyogenes and K. pneumoniae are the bacteria of choice to induce the pulmonary infection. Included in the studies are short-term single and multiple exposures as well as long-term exposures to gaseous pollutants such as O3 and NO2 and particulate pollutants such as sulfates and nitrates. Changes in the resistance are measured as excess mortalities and reduced survival time as compared to those in infected animals not exposed to the pollutants. Other parameters measured ranged from changes in the immune response to changes in retention rates of bacteria in lungs.

Aerosols↗
PubMed2006

The relationship between ambient air pollution and heart rate variability differs for individuals with heart and pulmonary disease.

Associations between concentrations of ambient fine particles [particulate matter < 2.5 microm aerodynamic diameter (PM2.5)] and heart rate variability (HRV) have differed by study population. We examined the effects of ambient pollution on HRV for 18 individuals with chronic obstructive pulmonary disease (COPD) and 12 individuals with recent myocardial infarction (MI) living in Atlanta, Georgia. HRV, baseline pulmonary function, and medication data were collected for each participant on 7 days in fall 1999 and/or spring 2000. Hourly ambient pollution concentrations were obtained from monitoring sites in Atlanta. The association between ambient pollution and HRV was examined using linear mixed-effect models. Ambient pollution had opposing effects on HRV in our COPD and MI participants, resulting in no significant effect of ambient pollution on HRV in the entire population for 1-, 4-, or 24-hr moving averages. For individuals with COPD, interquartile range (IQR) increases in 4-hr ambient PM2.5 (11.65 microg/m3)) and nitrogen dioxide (11.97 ppb) were associated with 8.3% [95% confidence interval (CI), 1.7-15.3%] and 7.7% (95% CI, 0.1-15.9%) increase in the SD of normal R-R intervals (SDNN), respectively. For individuals with MI, IQR increases in 4-hr PM2.5 (8.54 microg/m3) and NO2 (9.25 ppb) were associated with a nonsignificant 2.9% (95% CI, -7.8 to 2.3) and significant 12.1 (95% CI, -19.5 to -4.0) decrease in SDNN. Beta-blocker and bronchodilator intake and baseline forced expiratory volume in 1 sec modified the PM-SDNN association significantly, with effects consistent with those by disease group. Results indicate heterogeneity in the autonomic response to air pollution due to differences in baseline health, with significant associations for ambient NO2 suggesting an important role for traffic-related pollution.

Adrenergic beta-Antagonists↗
PubMed2006

The effects of air pollution on hospitalizations for cardiovascular disease in elderly people in Australian and New Zealand cities.

OBJECTIVE: The goal of this study was to estimate the associations between outdoor air pollution and cardiovascular hospital admissions for the elderly. DESIGN: Associations were assessed using the case-crossover method for seven cities: Auckland and Christchurch, New Zealand; and Brisbane, Canberra, Melbourne, Perth, and Sydney Australia. Results were combined across cities using a random-effects meta-analysis and stratified for two adult age groups: 15-64 years and >/= 65 years of age (elderly). Pollutants considered were nitrogen dioxide, carbon monoxide, daily measures of particulate matter (PM) and ozone. Where multiple pollutant associations were found, a matched case-control analysis was used to identify the most consistent association. RESULTS: In the elderly, all pollutants except O3 were significantly associated with five categories of cardiovascular disease admissions. No associations were found for arrhythmia and stroke. For a 0.9-ppm increase in CO, there were significant increases in elderly hospital admissions for total cardiovascular disease (2.2%) , all cardiac disease (2.8%), cardiac failure (6.0%), ischemic heart disease (2.3%), and myocardial infarction (2.9%). There was some heterogeneity between cities, possibly due to differences in humidity and the percentage of elderly people. In matched analyses, CO had the most consistent association. CONCLUSIONS: The results suggest that air pollution arising from common emission sources for CO, NO2, and PM (e.g., motor vehicle exhausts) has significant associations with adult cardiovascular hospital admissions, especially in the elderly, at air pollution concentrations below normal health guidelines. Relevance to clinical and professional practice: Elderly populations in Australia need to be protected from air pollution arising from outdoor sources to reduce cardiovascular disease.

Adolescent↗
PubMed2006

Traffic-related air pollution and otitis media.

BACKGROUND: Otitis media is one of the most common infections in young children. Although exposure to environmental tobacco smoke is a known risk factor associated with otitis media, little information is available regarding the potential association with air pollution. OBJECTIVE: We set out to study the relationship between exposure to traffic-related air pollution and otitis media in two birth cohorts. METHODS: Individual estimates of outdoor concentrations of traffic-related air pollutants-nitrogen dioxide, fine particles [particulate matter with aerodynamic diameters </= 2.5 microm (PM2.5)], and elemental carbon-were calculated for home addresses of approximately 3,700 and 650 infants from birth cohort studies in the Netherlands and Germany, respectively. Air pollution exposure was analyzed in relation to physician diagnosis of otitis media in the first 2 years of life. RESULTS: Odds ratios (adjusted for known major risk factors) for otitis media indicated positive associations with traffic-related air pollutants. An increase in 3 microg/m3 PM2.5, 0.5 microg/m3 elemental carbon, and 10 microg/m3 NO2 was associated with odds ratios of 1.13 (95% confidence interval, 1.00-1.27) , 1.10 (1.00-1.22) , and 1.14 (1.03-1.27) in the Netherlands and 1.24 (0.84-1.83) , 1.10 (0.86-1.41) , and 1.14 (0.87-1.49) in Germany, respectively. CONCLUSIONS: These findings indicate an association between exposure to traffic-related air pollutants and the incidence of otitis media. Given the ubiquitous nature of air pollution exposure and the importance of otitis media to children's health, these findings have significant public health implications.

Air Pollutants↗
PubMed1995

Associations between criteria air pollutants and asthma.

The evidence that asthma is increasing in prevalence is becoming increasingly compelling. This trend has been demonstrated not only in the United States, but also in the United Kingdom, New Zealand, Australia, and several other Western countries. In the United States, the increase is largest in the group under 18 years of age. There is mounting evidence that certain environmental air pollutants are involved in exacerbating asthma. This is based primarily on epidemiologic studies and more recent clinical studies. The U.S. Clean Air Act of 1970 provides special consideration to the class of outdoor air pollutants referred to as criteria pollutants, including O3, sulfur dioxide (SO2), particulate matter (PM), NOx, CO, and Pb. Standards for these pollutants are set by the U.S. Environmental Protection Agency with particular concern for populations at risk. Current evidence suggests that asthmatics are more sensitive to the effects of O3, SO2, PM, and NO2, and are therefore at risk. High SO2 and particulate concentrations have been associated with short-term increases in morbidity and mortality in the general population during dramatic air pollution episodes in the past. Controlled exposure studies have clearly shown that asthmatics are sensitive to low levels of SO2. Exercising asthmatics exposed to SO2 develop bronchoconstriction within minutes, even at levels of 0.25 ppm. Responses are modified by air temperature, humidity, and exercise level. Recent epidemiologic studies have suggested that exposure to PM is strongly associated with morbidity and mortality in the general population and that hospital admissions for bronchitis and asthma were associated with PM10 levels. In controlled clinical studies, asthmatics appear to be no more reactive to aerosols than healthy subjects. Consequently, it is difficult to attribute the increased mortality observed in epidemiologic studies to specific effects demonstrated in controlled human studies. Epidemiologic studies of hospital admissions for asthma have implicated O3 as contributing to the exacerbation of asthma; however, most study designs could not separate the O3 effects from the concomitant effects of acid aerosols and SO2. Controlled human clinical studies have suggested that asthmatics have similar changes in spirometry and airway reactivity in response to O3 exposure compared to healthy adults. However, a possible role of O3 in worsening atopic asthma has recently been suggested in studies combining allergen challenge following exposure to O3. Attempts at identification of factors that predispose asthmatics to responsiveness to NO2 has produced inconsistent results and requires further investigation. In summary, asthmatics have been shown to be a sensitive subpopulation relative to several of the criteria pollutants. Further research linking epidemiologic, clinical, and toxicologic approaches is required to better understand and characterize the risk of exposing asthmatics to these pollutants.

Adolescent↗
PubMedDate not supplied

Air pollution and health in urban areas.

In this paper, recent reviews of the World Health Organization, other review papers, and more recent literature on the human health effects of current air pollution trends in urban areas are reviewed and summarized as follows: Sulphur dioxide. Some studies, but not others, found associations between sulphur dioxide (SO2) exposure and daily mortality and morbidity. Single-pollutant correlations sometimes disappeared when other pollutants, especially suspended particulate matter (SPM), were included. Cross-sectional studies with asthmatics revealed significant, non-threshold relations between SO2 and decrements of the forced expiratory volume in 1 second (FEV1). Nitrogen dioxide. Weak associations between short-term nitrogen dioxide (NO2) exposure from gas cooking and respiratory symptoms and a decrement in lung function parameters were found in children, but not consistently in exposed women. With long-term exposure, children, but not adults, exhibit increased respiratory symptoms, decreased lung function, and increased incidences of chronic cough, bronchitis, and conjunctivitis. A causal relationship between NO2 exposure and adverse health effects has not yet been established. Carbon monoxide. Binding of CO in the lungs with hemoglobin in the blood forms carboxyhemoglobin (COHb), which impairs the transport of oxygen. The health effects of CO include hypoxia, neurological deficits and neurobehavioral changes, and increases in daily mortality and hospital admissions for cardiovascular diseases. The latter persists even at very low CO levels, indicating no threshold for the onset of these effects. Whether the relation between daily mortality and exposure to CO are causal or whether CO might act as a proxy for SPM is still an open question. Ambient CO may have even more serious health consequences than does COHb formation and at lower levels than that mediated through elevated COHb levels. Ozone. Short-term acute effects of O3 include pulmonary function decrements, increased airway responsiveness and airway inflammation, aggravation of pre-existing respiratory diseases like asthma, increases in daily hospital admissions and emergency department visits for respiratory causes, and excess mortality. Exposure-response relations are non-linear for the respective associations between O3 and FEV1, inflammatory changes, and changes in hospital admissions, whereas the relation between percent change in symptom exacerbation among adults and asthmatics is linear. Single-pollutant associations between O3 exposure and daily mortality and hospital admissions for respiratory diseases is statistically significant, even in multi-pollutant models. Suspended particulate matter. Associations between SPM concentrations and mortality and morbidity rates are significant. The acute health effects of SPM, even at short-term low levels of exposure, include increased daily mortality and hospital admission rates for exacerbation of respiratory disease, fluctuations in the prevalence of bronchodilator use, and cough and peak flow reductions, as well as long-term effects with respect to mortality and respiratory morbidity. Such effects depend on particle size and concentration and can fluctuate with daily fluctuations in PM10 or PM2.5 levels. The relation between PM10 or PM2.5 exposure and acute health effects is linear at concentrations below 100 micrograms/m3. Currently no threshold has been reported below which no effects occur. The influence of co-polluting gaseous pollutants could explain part of the observed variance in short-term health effects and reduce the contribution of SPM. Lead. The biological effects of lead can be related to blood lead levels, the best indicator of internal exposure. The potential effects of lead in adults and children include encephalopathic signs and symptoms, central nervous system symptoms, cognitive effects, increased blood pressure, and reduced measures of child intelligence. (ABSTRACT TRUNCATED)

Adult↗