Nutrient utilization by sheep and performance and carcass characteristics of steers fed crab waste-straw silage

Exacerbations of asthma have been associated with exposure to ozone or particles with a 50% cut-off aerodynamic diameter of 10 microm (PM10). We postulated in this study that the association of summertime air pollution (i.e. ozone and PM10) with acute respiratory symptoms, medication use and peak expiratory flow differs among patients grouped according to asthma severity. During the summer of 1995, effects of ambient air pollution on these parameters were studied in a panel of 60 nonsmoking patients with intermittent to severe persistent asthma. These patients were recruited from our Pulmonary Out-patient Clinic. Subgroup analysis was performed on the degree of hyperresponsiveness and lung steroid use before the start of the study, as indictors for the severity of asthma. Associations of the parameters studied with ozone, PM10, nitrogen dioxide (NO2), sulphur dioxide (SO2) and black smoke were evaluated using time series analysis. Several episodes with increased summertime air pollution occurred during the 96 day study period. Eight hour average ozone concentrations exceeded the World Health Organization (WHO) Air Quality Guidelines (120 microg x m(-3)) on 16 occasions. Daily mean levels of PM10 were moderately elevated (range 16-98 microg x m(-3)). Levels of the other measured pollutants were low. There was a consistent, positive association of the prevalence of shortness of breath (maximal relative risk (RRmax) 1.18) with ozone, PM10, black smoke and NO2. In addition, bronchodilator use was associated with both ozone and PM10 levels (RRmax 1.16). Stratification by airway hyperresponsiveness and steroid use did not affect the magnitude of the observed associations. No associations with peak expiratory flow measurements were found. We conclude that the severity of asthma is not an indicator for the sensitivity to air pollution.     

Urban air pollution and cardiopulmonary ill health: a 14.5 year time series study

OBJECTIVES: To examine possible associations between daily concentrations of urban air pollutants and hospital emergency admissions and mortality due to cardiac and pulmonary disease. METHODS: A time series study was conducted in the City of Edinburgh, which has a population of about 450,000. Poisson log linear regression models were used to investigate the relation of the daily event rate with daily air pollution concentrations of sulphur dioxide (SO2) and black smoke from 1981 to 1995, and of nitrogen dioxide (NO2), ozone (O3), carbon monoxide (CO), and particulate matter (PM10) from 1992 to 1995. Adjustments were made for seasonal and weekday variation, daily temperature, and wind speed. RESULTS: The most significant findings were positive associations over the period 1981-95 between black smoke as a mean of the previous three days and daily all cause mortality in people aged > or = 65, and respiratory mortality also in this age group (3.9% increase in mortality for a 10 micrograms/m3 increment in black smoke). For hospital emergency admissions between 1992 and 1995 the two most significant findings (p < 0.05) were for cardiovascular admissions of people aged > or = 65 which showed a positive association with PM10 as a mean of the 3 previous days, and a negative association with O3 as a mean of the previous three days. Analyses of outcomes based on linkage with previous cardiorespiratory emergency admissions did not show substantially different results. CONCLUSION: These data suggest that in the City of Edinburgh, after correction for confounders, there was a small but significant association between concentrations of black smoke and respiratory mortality in the older age group, probably attributable to higher pollution levels in the early part of the study period. There were also generally weak and variable associations between day to day changes in concentrations of urban air pollutants at a single central point and emergency hospital admission rates from cardiac and respiratory disease.     

Air pollution and allergy: experimental studies on modulation of allergen release from pollen by air pollutants

The fact that allergic diseases increase in prevalence is a generally accepted and worldwide phenomenon. The causes for this increase are not known: only hypothetical concepts exist. Epidemiological studies comparing Eastern and Western European populations have shown a striking difference in the prevalence of respiratory atopic diseases, which is lower in the East. At the same time, different patterns of air pollution have been described, namely 'classical' type I, characterized by SO2 and dust prevailing in the East, and 'modern' type II, characterized by organic compounds, fine particles and ozone, which is more prominent in the West. Type II was associated in multivariate regression analysis with increased prevalence of IgE-mediated allergy. Pollen grains collected from industrial regions with high polyaromatic hydrocarbon load in West Germany, but not in East Germany, were shown to be agglomerated with airborne particles. In vitro exposure of pollen to particles indicated morphological changes and increased allergen release from the pollen. In vitro exposure of pollen to gaseous pollutants (SO2 and NO2) under different conditions of humidity resulted in SO2-induced, but not NO2-induced reduction of allergen release from pollen. It is concluded that the bioavailability of grass pollen allergens may be modulated by air pollutants, supporting the concept of an interaction between pollen and pollutants in the atmosphere outside the organism which in turn may affect allergy-relevant phenomena.     

Intestinal absorption and analgesic activity of aminopeptidase-resistant cellobiose-coupled leucine enkephalinamide

OBJECTIVES: To assess the relation between several daily indicators of air pollution (particulates and gases) and daily mortality in the metropolitan area of Rome and in the central part of the city. METHODS: Time series analysis. The associations between daily concentrations of pollutants (particles, SO2, NO2, CO, O3) recorded by five fixed monitors and daily total mortality in the period from January 1992 to June 1995 were evaluated. The analysis included examination of the pollution effect on mortality by place of residence within the metropolitan area, by season, age, place of death (in and out a hospital), and cause of death (cardiovascular and respiratory disease). The Poisson model included loses smooth functions of the day of study, mean temperature, mean humidity, and indicator variables for day of the week and holidays. RESULTS: The mean daily number of deaths was 56.9 (44.8 among people > or = 65 years old). A mean of 36.3 deaths occurred in the city centre; 37.3 deaths a day were recorded in a hospital. Total mortality was significantly associated with a 10 micrograms/m3 increase in particles (0.4%) on that day (log 0), and with a 10 micrograms/m3 increase in NO2 at lag 1 (0.3%) and lag 2 (0.4%) (1 and 2 days before, respectively). The effect of particles (lag 0) and of NO2 (lag 2) on total mortality was higher among those living in the city centre (0.7% and 0.5%, respectively). The risk estimates were higher in the warmer season (1.0% and 1.1%, respectively), whereas no difference was found for those dying in or out of the hospital. The effect of particles was robust to a sensitivity analysis and to the inclusion of NO2 in the regression model. CONCLUSIONS: Increase in particulates and NO2, generated by the same mobile combustion sources, is associated with a short term increase in mortality in Rome. The effect is more evident among residents in the city centre, where the levels of exposure to pollutants recorded by fixed monitors are probably more reliable indicators of personal exposure.     

Effects of photochemical air pollution and allergen exposure on upper respiratory tract inflammation in asthmatics

Asthma is an inflammatory disease of the airways, and exacerbations of this disease have been associated with high levels of air pollution. The objective of this study was to examine whether ambient air pollution and/or allergen exposure induces inflammatory changes in the upper airways of asthmatics. Sixty patients with intermittent to severe persistent asthma visited the Hospital's Out Patient Clinic every 2 wk for a period of 3 mo, and on each visit a nasal lavage was obtained. Associations between nasal inflammatory parameters and seasonal allergens and/or air pollution exposures were analyzed using linear regression analysis. The study ran from July 3 to October 6, 1995, during which period ozone (8-h mean: 80 micrograms/m3) and PM10 (24-h mean: 40 micrograms/m3) were the major air pollutants; the major aeroallergen was mugwort pollen (24-h mean: 27 pollen grains/m3). Effects on both cellular and soluble markers in nasal lavage were demonstrated for both ozone and mugwort pollen, but not for PM10. Ambient ozone exposure was associated with an increase in neutrophils (112% per 100 micrograms/m3 increase in 8-h average ozone concentration), eosinophils (176%), epithelial cells (55%), IL-8 (22%), and eosinophil cationic protein (ECP) (19%). Increases in environmental mugwort pollen counts were associated with an increase in nasal eosinophils (107% per 100 pollen/m3) and ECP (23%), but not with neutrophils, epithelial cells, or lL-8. This study demonstrated that both ambient ozone and allergen exposure are associated with inflammatory responses in the upper airways of subjects with asthma, although the type of inflammation is qualitatively different.     

Subclasses of LpA-I in coronary artery disease: distribution and cholesterol efflux ability

To determine the effect of air pollution in Mexico City on respiratory health, patient visits for upper respiratory tract infections were monitored in five clinics. Levels of ozone, nitrogen dioxide, carbon monoxide, and sulfur dioxide, and climatological variables were collected. Correlations of filtered data revealed an association between NO2 and O3 with an increase in visits to clinics because of respiratory problems. Autoregressive analysis indicated that pollutant levels/respiratory visits associations remained significant even after simultaneous inclusion of temperature, suggesting that air pollution was associated with 10 to 16% of the clinic visits. The relative risk indicated that high levels of O3 and NO2 could increase the total number of clinic visits to between 19 and 43% above average. The other pollutants and the control group did not demonstrate significant associations.     

Association between ozone and asthma emergency department visits in Saint John, New Brunswick, Canada

This study examines the relationship of asthma emergency department (ED) visits to daily concentrations of ozone and other air pollutants in Saint John, New Brunswick, Canada. Data on ED visits with a presenting complaint of asthma (n = 1987) were abstracted for the period 1984-1992 (May-September). Air pollution variables included ozone, sulfur dioxide, nitrogen dioxide, sulfate, and total suspended particulate (TSP); weather variables included temperature, humidex, dewpoint, and relative humidity. Daily ED visit frequencies were filtered to remove day of the week and long wave trends, and filtered values were regressed on air pollution and weather variables for the same day and the 3 previous days. The mean daily 1-hr maximum ozone concentration during the study period was 41.6 ppb. A positive, statistically significant (p < 0.05) association was observed between ozone and asthma ED visits 2 days later, and the strength of the association was greater in nonlinear models. The frequency of asthma ED visits was 33% higher (95% CI, 10-56%) when the daily 1-hr maximum ozone concentration exceeded 75 ppb (the 95th percentile). The ozone effect was not significantly influenced by the addition of weather or other pollutant variables into the model or by the exclusion of repeat ED visits. However, given the limited number of sampling days for sulfate and TSP, a particulate effect could not be ruled out. We detected a significant association between ozone and asthma ED visits, despite the vast majority of sampling days being below current U.S. and Canadian standards.     

Long-term inhalable particles and other air pollutants related to mortality in nonsmokers

Long-term ambient concentrations of inhalable particles less than 10 microm in diameter (PM10) (1973- 1992) and other air pollutants-total suspended sulfates, sulfur dioxide, ozone (O3), and nitrogen dioxide-were related to 1977-1992 mortality in a cohort of 6,338 nonsmoking California Seventh-day Adventists. In both sexes, PM10 showed a strong association with mortality for any mention of nonmalignant respiratory disease on the death certificate, adjusting for a wide range of potentially confounding factors, including occupational and indoor sources of air pollutants. The adjusted relative risk (RR) for this cause of death as associated with an interquartile range (IQR) difference of 43 d/yr when PM10 exceeded 100 microg/m3 was 1.18 (95% confidence interval [CI]: 1.02, 1.36). In males, PM10 showed a strong association with lung cancer deaths-RR for an IQR was 2.38 (95% CI: 1.42, 3.97). Ozone showed an even stronger association with lung cancer mortality for males with an RR of 4.19 (95% CI: 1.81, 9.69) for the IQR difference of 551 h/yr when O3 exceeded 100 parts per billion. Sulfur dioxide showed strong associations with lung cancer mortality for both sexes. Other pollutants showed weak or no association with mortality.     

Increased plasma viscosity during an air pollution episode: a link to mortality?

BACKGROUND: Air pollution episodes have been consistently associated with increased mortality, and most strikingly with mortality due to cardiovascular disease. One hypothesis to explain this association is that inflammation of the peripheral airways caused by pollution might increase blood coagulability. We have tested this hypothesis in a cross-sectional study by comparing measurements of plasma viscosity during a severe episode of air pollution during 1985 with those made on less polluted days. METHODS: Plasma viscosity was measured as part of the MONICA Augsburg survey during the winter of 1984-85 in 3256 randomly selected men and women aged 25-64 years. Daily mean concentrations of air pollutants and meteorological variables were measured in Augsburg as part of the automated Bavarian air-quality network. We compared measurements of plasma viscosity made in 324 people who attended for screening during the pollution episode and in 2932 people screened during the remainder of the survey period. FINDINGS: In January, 1985, high concentrations of sulphur dioxide (mean 200 micrograms/m3) and total suspended particles (mean 98 micrograms/m3) were recorded during a 13-day period in Augsburg. In men, the odds ratio for plasma viscosity above the 95th percentile of the distribution (1.38 mPa s) was 3.6 (95% CI 1.6-8.1) comparing measurements during the air pollution episode with non-episode measurements after adjustment for cardiovascular risk factors and meteorological variables. The corresponding odds ratio for women (95th percentile of plasma viscosity 1.37 mPa s) was 2.3 (1.0-5.3). High concentrations of carbon monoxide were also associated with increased plasma viscosity in women. INTERPRETATION: During the 1985 air pollution episode, an increased risk of extreme values of plasma viscosity was observed in both men and women. Altered blood rheology due to inflammatory processes in the lung that induce an acute-phase reaction might therefore be part of the pathological mechanisms linking air pollution to mortality.     

Air pollution and asthma

The role of air pollution in the increased prevalence and morbidity of asthma has been widely debated, but results to date indicate that the normally encountered levels of air pollution are unlikely to contribute to a worsening of asthma. When the levels of sulphur dioxide (SO2) are exceptionally high it is possible that asthmatic patients may have increased symptoms after exertion, since this irritant gas acts as a trigger to bronchoconstriction. There is also evidence that suspended particles may also act as an inciter of asthma symptoms when concentrations are high. Experimentally, ozone in high concentrations may increase airway responsiveness in both normal and asthmatic subjects by inducing airway inflammation, but asthmatic individuals show the same responses as normal subjects and there is little or no evidence to link increases in ambient ozone with an increase in asthma. There is little evidence that nitrogen dioxide (NO2), even at the peak levels recorded, has any significant effect on airway function in normal or asthmatic individuals. Other air pollutants which are present in lower concentrations have not been studied as extensively, but there is no convincing evidence that they cause significant respiratory symptoms in asthmatic patients. It is still possible that combinations of air pollutants may have greater effects on airway function than exposure to a single pollutant, although there is little evidence to support this. Epidemiological evidence provides little support for the idea that atmospheric pollution levels are related to the frequency of asthma symptoms or the frequency of attacks. More importantly, there is no evidence that asthma prevalence or aetiology is related to the level of air pollution. A review of currently available information therefore provides little evidence for the widely expressed view that atmospheric pollution is related to increased prevalence or morbidity of asthma or is related to the causation of asthma.     

Oxygen saturation, pulse rate, and particulate air pollution: A daily time-series panel study

Although epidemiological studies have linked particulate air pollution with cardiopulmonary mortality, underlying biological mechanisms remain largely unknown. Unexplored pathophysiological pathways include transient declines in blood oxygenation and/or changes in cardiac rhythm following particulate exposure. In this study, blood oxygen saturation using pulse oximetry (SpO2) and pulse rate were measured daily on a panel of 90 elderly subjects during the winter of 1995-1996 in Utah Valley. Associations of SpO2 and pulse rate with respirable particulate pollution (particles with an aerodynamic diameter 相似文献   

Bupivacaine 0.01% and/or epinephrine 0.5 microg/ml improve epidural fentanyl analgesia after cesarean section

The Pollution Effects on Asthmatic Children in Europe (PEACE) study is a multicentre study of the acute effects of particles with a 50% cut-off aerodynamic diameter of 10 microm (PM10), black smoke (BS), sulphur dioxide (SO2) and nitrogen dioxide (NO2) on the respiratory health of children with chronic respiratory symptoms. The study was conducted in the winter of 1993/1994 by 14 research centres in Europe. A total of 2,010 children, divided over 28 panels in urban and suburban locations, was followed for at least 2 months. Exposure to air pollution was monitored on a daily basis. Health status was monitored by daily peak expiratory flow (PEF) measurements and a symptom diary. The association between respiratory health and air pollution levels was calculated with time series analysis. Combined effect estimates of air pollution on PEF or the daily prevalence of respiratory symptoms and bronchodilator use were calculated from the panel-specific effect estimates. Fixed effect models were used and, in cases of heterogeneity, random effect models. No clear associations between PM10, BS, SO2 or NO2 and morning PEF, evening PEF, prevalence of respiratory symptoms or bronchodilator use could be detected. Only previous day PM10 was negatively associated with evening PEF, but only in locations where BS was high compared to PM10 concentrations. There were no consistent differences in effect estimates between subgroups based on urban versus suburban, geographical location or mean levels of PM10, BS, SO2 and NO2. The lack of association could not be attributed to a lack of statistical power, low levels of exposure or incorrect trend specifications. In conclusion, the PEACE project did not show effects of particles with a 50% cut-off aerodynamic diameter of 10 microm, black smoke, sulphur dioxide or nitrogen dioxide on morning or evening peak expiratory flow or the daily prevalence of respiratory symptoms and bronchodilator use.     

Airborne small particles as a cause of pulmonary diseases and excessive mortality?

The paper reviews the available literature with regard to human health effects of fine particulate matter (PM10, PM2.5) from a Danish perspective. Fine particulate matter is not routinely measured in any Danish air pollution monitoring programme. Preliminary surveys show elevated PM2.5 levels in Copenhagen corresponding to levels found in other cities in Europe and the USA, and a close relationship between outdoor and indoor concentrations. It has been roughly estimated that about 400 people in the Greater Copenhagen area may suffer a premature death due to airborne fine particulate matter. A limited number of Danish studies support the view that health effects (respiratory symptoms and increased medication) can be observed in sensitive city populations at air pollution levels well below international air quality standards.     

基于机器学习的北京市PM2.5浓度预测模型及模拟分析

对北京市周边8个点多个压力高度的温度、湿度和风速数据, 以及北京市PM2.5污染数据进行了分析和归一化处理, 建立了反向传播神经网络(back propagation, BP)、卷积神经网络(convolutional neural network, CNN) 和长短期记忆模型(long short-term memory, LSTM) 对上述气象数据和污染数据进行训练, 训练结果表明: 反向传播神经网络模型和卷积神经网络模型对未来1 h的PM2.5污染等级的预测准确率较低, 而长短期记忆模型的准确率较高.使用长短期记忆模型预测未来1 h的PM2.5污染值与实际值十分接近, 表明北京市的PM2.5污染与其周边地区的气象条件关系密切.通过利用长短期记忆模型对不同压力高度的气象数据进行训练和对比, 得出在利用气象数据预测污染时, 仅使用近地面气象数据比使用多个高度上的气象数据更加准确.      

An association between air pollution and mortality in six U.S. cities

BACKGROUND: Recent studies have reported associations between particulate air pollution and daily mortality rates. Population-based, cross-sectional studies of metropolitan areas in the United States have also found associations between particulate air pollution and annual mortality rates, but these studies have been criticized, in part because they did not directly control for cigarette smoking and other health risks. METHODS: In this prospective cohort study, we estimated the effects of air pollution on mortality, while controlling for individual risk factors. Survival analysis, including Cox proportional-hazards regression modeling, was conducted with data from a 14-to-16-year mortality follow-up of 8111 adults in six U.S. cities. RESULTS: Mortality rates were most strongly associated with cigarette smoking. After adjusting for smoking and other risk factors, we observed statistically significant and robust associations between air pollution and mortality. The adjusted mortality-rate ratio for the most polluted of the cities as compared with the least polluted was 1.26 (95 percent confidence interval, 1.08 to 1.47). Air pollution was positively associated with death from lung cancer and cardiopulmonary disease but not with death from other causes considered together. Mortality was most strongly associated with air pollution with fine particulates, including sulfates. CONCLUSIONS: Although the effects of other, unmeasured risk factors cannot be excluded with certainty, these results suggest that fine-particulate air pollution, or a more complex pollution mixture associated with fine particulate matter, contributes to excess mortality in certain U.S. cities.     

PM2.5 and mortality in long-term prospective cohort studies: cause-effect or statistical associations?

Concentrations of ambient PM2.5 (particulate matter <2.5 microm in aerodynamic diameter) were associated with increased mortality in two prospective cohort studies. In this paper, I assess whether the weight of the evidence supports a causal association. I assumed the study population in each city to have the same exposure; therefore, these are ecologic studies because exposure is at the group level. Health outcome and confounding data are at the individual level. Ambient PM concentrations are inadequate surrogates for personal exposure because they are at the group level and comprise only a small proportion of personal exposure, they change over time, and they constitute only a small proportion of a life span. The strength of association and exposure-response relationships cannot be determined because the ecologic group-level risks of PM2.5 are overestimated 150- to 300-fold based on an analogy with individual-level exposure to inhaled cigarette smoke. Risk estimates may also be high because of confounding from factors such as physical activity and lung function. The evidence is not coherent because the stronger associations are expected to be with morbidity, but instead are with mortality. For example, PM2.5 was associated with mortality but not with measurable reductions in lung function. Biological plausibility is lacking because lifetime exposure of rats to combustion products at concentrations two to three orders of magnitude higher than air pollution levels cause lung overloading but no consistent reduction in survival. Criteria for quantitative risk assessment are not met so the data are not useful for setting air quality standards. The weight of evidence suggests there is no substantive basis for concluding that a cause-effect relationship exists between long-term ambient PM2.5 and increased mortality.     

Asthma and exacerbation of chronic bronchitis: sentinel and environmental data in a time series analysis

To see whether effects of air pollutants and other environmental factors on the respiratory tract can be detected by the Swiss sentinel reporting system, two years' data of asthma bronchiale and exacerbation of chronic bronchitis were analyzed. On average, 16 cases of asthma and 9 cases of bronchitis were reported per week. The respective figures expressed as mean percentages of all consultations were 0.12% and 0.065%. Data of SO2, NO2, ozone and total suspended particles were used to measure air pollution. Additionally, meteorologic parameters such as air temperature and atmospheric pressure were used, as well as the appearance of the most important pollen groups in Switzerland: grass, birch tree and mugwort. Environmental data were summarized using the mean or sum of all measuring stations. Autocorrelations in the time series were accounted for statistically. Our analysis could not establish any relationship between reports of asthma or exacerbation of chronic bronchitis and air pollutants or other environmental data. This result, which is partly contradicted by the literature, could be explained by low numbers of reports due to patient's self administration of medication and an imprecise determination of true exposure.     

Pollution and allergy: the contributions of animal and in vitro experimentation

The respiratory pathological symptoms induced by atmospheric pollutants are closely dependent on the action of the aerocontaminants on the cells of the respiratory tract that are exposed to their effects. Two methods of experimental investigation are used to specify the effects of pollutants on the respiratory system: Study of the morphological and functional alterations of animal respiratory systems after exposure to different pollution constituents. Exposure of bronchitic or pulmonary cells to microquantities of pollutants, using different techniques that create direct contact between the pollutant and target cells. In animals gaseous pollutants alter the means of defence (muco-ciliary purification and antibacterial defence), inducing development of a neutrophil inflammatory reaction and, for ozone and NO2 favouring sensitisation by allergen-dependent IgE; diesel particles are responsible for restrictive ventilation problems, an inflammatory reaction, a sensitisation develops to pneumoallergens and in some cases of the development of pulmonary tumours. In vitro studies specify the cellular mechanisms and the molecules that are responsible for the observed phenomena: increase in the synthesis and expression of messenger DNA the codes for the pro-inflammatory cytokines, adherance molecules and chimiokines.     

Acute effects of inhaled urban particles and ozone: lung morphology, macrophage activity, and plasma endothelin-1

We studied acute responses of rat lungs to inhalation of urban particulate matter and ozone. Exposure to particles (40 mg/m3 for 4 hours; mass median aerodynamic diameter, 4 to 5 microm; Ottawa urban dust, EHC-93), followed by 20 hours in clean air, did not result in acute lung injury. Nevertheless, inhalation of particles resulted in decreased production of nitric oxide (nitrite) and elevated secretion of macrophage inflammatory protein-2 from lung lavage cells. Inhalation of ozone (0.8 parts per million for 4 hours) resulted in increased neutrophils and protein in lung lavage fluid. Ozone alone also decreased phagocytosis and nitric oxide production and stimulated endothelin-1 secretion by lung lavage cells but did not modify secretion of macrophage inflammatory protein-2. Co-exposure to particles potentiated the ozone-induced septal cellularity in the central acinus but without measurable exacerbation of the ozone-related alveolar neutrophilia and permeability to protein detected by lung lavage. The enhanced septal thickening was associated with elevated production of both macrophage inflammatory protein-2 and endothelin-1 by lung lavage cells. Interestingly, inhalation of urban particulate matter increased the plasma levels of endothelin-1, but this response was not influenced by the synergistic effects of ozone and particles on centriacinar septal tissue changes. This suggests an impact of the distally distributed particulate dose on capillary endothelial production or filtration of the vasoconstrictor. Overall, equivalent patterns of effects were observed after a single exposure or three consecutive daily exposures to the pollutants. The experimental data are consistent with epidemiological evidence for acute pulmonary effects of ozone and respirable particulate matter and suggest a possible mechanism whereby cardiovascular effects may be induced by particle exposure. In a broad sense, acute biological effects of respirable particulate matter from ambient air appear related to paracrine/endocrine disruption mechanisms.