[Air pollution and cardiovascular and cerebrovascular disease: Epidemiologic data]. / Pollution de l'air et pathologie athérothrombotique cardiaque et cérébrale: Données épidémiologiques.

Recent convergent data suggest that air pollution affects the risk of acute atherothrombotic events including both myocardial infarction and ischemic stroke. The principal epidemiologic studies begun in the 1990s first examined the respiratory effects of atmospheric pollution and then focused on how pollution peaks affected cardiovascular risk. These studies used data from large metropolitan areas in North America and Asia as well as several large European cities to demonstrate the clear existence of a relation between air pollution and cardio- and cerebrovascular mortality. They also observed an increase in hospital admissions for myocardial infarctions and cerebrovascular accidents on days with high air pollution levels. The pollutants involved have not yet been clearly designated, but it appears that fine suspended particulate matter (PM2.5) and gaseous pollutants such as ozone appear to contribute strongly to these harmful effects. A complete analysis of these data shows the need for a thorough evaluation of the cardio- and cerebrovascular risks associated with air pollution, especially in French metropolitan areas. Precise identification of those at high risk from specific pollutants is essential to improve targeting of prevention strategies.

Assessing exposure to diesel exhaust particles: a case study.

The assessment of the vehicular contributions to urban pollution levels is of particular importance given the current interest in the possible adverse health effects. This study focused on human exposure to diesel-engine-derived particulate matter. Diesel vehicles are known to emit fine particulate matter (PM2.5) containing carcinogens such as polycyclic aromatic hydrocarbons (PAHs), and have therefore received considerable attention. In this study, the physical (mass and number concentration, and size distribution) and chemical (PAHs) properties were investigated at a major bus interchange in Singapore, influenced only by diesel exhausts. Number concentration and size distribution of particles were determined in real time, while the mass concentrations of PM2.5, and PAHs were measured during operating and nonoperating hours. The average mass concentrations of PM2.5 and PAHs increased by a factor of 2.34 and 5.18, respectively, during operating hours. The average number concentration was also elevated by a factor of 5.07 during operating hours. This increase in the concentration of PM2.5 particles and their chemical constituents during operating hours was attributable to diesel emissions from in-use buses based on the particle size analysis, correlation among PAHs, and the commonly used PAHs diagnostic ratios. To evaluate the potential health threat due inhalation of air pollutants released from diesel engines, the incremental lifetime cancer risk was also calculated for a maximally exposed individual. The findings indicate that the air quality at the bus interchange poses adverse health effects.

Spatiotemporal features of severe air pollution in northern Taiwan.

BACKGROUND, AIMS AND SCOPE: This research attempted to identify the dominant factors simultaneously affecting the airborne concentrations of five air pollutants with principal component analysis and to determine the meteorologically related parameters that cause severe air-pollution events. According to the definition of subPSI and PSI values through the U.S. EPA, the historical raw data of five criteria air pollutants, SO2, CO, O3, PM10 and NO2, were calculated as daily subPSI values. In addition to the airborne concentrations, this study simultaneous collected the surface meteorological parameters of the Taipei meteorological station, established by the Central Weather Bureau. METHODS: Principal component analysis was conducted to screen severe air pollution scenarios for five air pollutants: SO2, CO, O3, PM10 and NO2. The concentrations of various air pollutants measured at 17 air-quality stations in northern Taiwan from 1995 to 2001 were transformed into daily subPSI values. The correlation analysis of the five air pollutants and four meteorological parameters (wind speed, temperature, mixing height and ventilation rate) were included in this research. After screening severe air pollution scenarios, this study recognized the synoptic patterns easily causing the severe air-pollution events. RESULTS AND DISCUSSION: Analytical results showed that the eigenvalues of the first two principal components for SO2, CO, O3, PM10 and NO2 were greater than 1. The first component of five air pollutants explained 64, 64, 67, 76 and 63% of subPSI variance for SO2, CO, O3, PM10 and NO2, respectively. Only the correlation coefficient of NO2 and CO had statistically significant positive values (0.82); other pollutant pairs presented medium (0.4 to 0.7) or low (0 to 0.4) positive values. The correlation coefficients for air pollutants and three meteorological parameters (wind speed, mixing height and ventilation index) were medium or low negative values. In northern Taiwan, spring was most likely induced high concentrations and the component scores of the first component for SO2, CO, PM10 and NO2; summer was the worst season that caused high O3 episodes. Consequently, the analytical results of factor loadings for the first principal component and emission inventory of various sources revealed that mobile sources were dominant factors affecting ambient air quality in northern Taiwan. CONCLUSION: According to the results of principal component analysis for the five air pollutants, the first two of 17 components were cited as major factors and explained 71% of subPSI variance. Based on the inventory of NOx emissions and the isopleth diagram of factor loading for the first component, mobile sources in the southwest Taipei City accounted for the highest factor loading values and emission inventory values. Synoptic analysis and principal component analysis demonstrated that three types of weather patterns (high-pressure recirculation, prefrontal warm sector and the southwesterly wind system) easily caused the severe air-pollution scenarios. In summary, if severe air-pollution days occurred, the average meteorological parameters experienced adverse conditions for diffusing air pollutants; that is, the average values of wind speed, mixing height and ventilation index were lower than 2.1 ms(-1), 360 m and 800 m2s(-1), respectively. If one of the three synoptic patterns were to occur in combination with adverse meteorological conditions, severe air-pollution events would be developed. RECOMMENDATION AND OUTLOOK: By utilizing synoptic patterns, this work found three weather systems easily caused severe air-pollution events over northern Taiwan. Analytical results showed, respectively, the wind speed and mixing height were less than 2.1 m/s and 360 m during severe air-pollution events.

Phase II enzymes induction blocks the enhanced IgE production in B cells by diesel exhaust particles.

Oxidant pollutants such as diesel exhaust particles (DEPs) can initiate and exacerbate airway allergic responses through enhanced IgE production. These effects are especially pronounced in individuals in whom phase II antioxidant enzyme responses are impaired. We confirmed that DEPs and DEP extracts (DEPX) can act directly on B lymphocytes and showed that DEPX could enhance IgH epsilon germline transcription in a B cell line and in PBMCs. We therefore studied the regulation in B cells of NAD(P)H: quinone oxidoreductase (NQO1) as a typical model phase II enzyme and its role in modulating DEPX-enhanced IgE responses. DEPX increased NQO1 mRNA expression in a dose-dependent manner. NQO1 protein induction by DEPX was confirmed by Western blot. DEPs induced activity of the antioxidant response element located in the NQO1 gene promoter. Induction of both NQO1 mRNA and protein expression could be blocked by coculture with an antioxidant and partly repressed by inhibitors of PI3K and p38 MAPK, but not by inhibitors of MAPK/ERK kinase (MEK/ERK) or protein kinase C. The ability of DEPX to enhance IgE production was blocked by the induction of phase II enzymes, including NQO1 in B cells by the chemical sulforaphane. These findings suggest that a natural protective mechanism in B cells from oxidant pollutants such as diesel particles is the expression of phase II enzymes through induction of antioxidant response elements and support the approach of overexpression of these enzymes as a potential future chemopreventative strategy.

Nasal responses in asthmatic and nonasthmatic subjects following exposure to diesel exhaust particles.

Asthma rates have been increasing worldwide, and exposure to diesel exhaust particles (DEP) may be implicated in this increase. DEP may also play a role in the increased morbidity and mortality associated with ambient airborne particulate matter (PM) exposure. Two types of nasal responses have been reported for human subjects nasally instilled with one type of DEP: alterations in cytokines responses, and an increase in immunoglobulin E (IgE) production. Since DEP composition can vary depending on several factors, including fuel composition and engine load, the ability of another DEP particle and ozone-treated DEP to alter nasal IgE and cytokine production was examined. Nonasthmatic and asthmatic subjects were intranasally instilled with 300 microg NIST 1650 DEP per nostril, NIST 1650 DEP previously exposed to ozone (ozDEP; 300 microg/nostril), or vehicle. Subjects underwent nasal lavage before DEP exposure, and 4 and 96 h after exposure. Nasal cell populations and soluble mediators in the nasal lavage fluid were characterized. Total cell number, cell types, cell viability, concentrations of soluble mediators (including interleukin [IL]-8, IL-6, IgE, and granulocyte-macrophage colony-stimulating factor [GM-CSF]) were not altered by either DEP or ozDEP exposure. NO levels were not altered by either particle exposure. These findings suggest that DEP can be relatively noninflammatory and nontoxic, and that the physicochemical characteristics of DEP need to be considered when assessing the health effects of exposure to diesel exhaust.

PM2.5 constituents and related air quality variables as predictors of survival in a cohort of U.S. military veterans.

Air quality data on trace metals, other constituents of PM2.5, and criteria air pollutants were used to examine relationships with long-term mortality in a cohort of male U.S. military veterans, along with data on vehicular traffic density (annual vehicle-miles traveled per unit of land area). The analysis used county-level environmental data for the period 1997-2002 and cohort mortality for 1997-2001. The proportional hazards model included individual data on age, race, smoking, body mass index, height, blood pressure, and selected interactions; contextual variables also controlled for climate, education, and income. In single-pollutant models, traffic density appears to be the most important predictor of survival, but potential contributions are also seen for NO2, NO3-, elemental carbon, nickel, and vanadium. The effects of the other main constituents of PM2.5, of crustal particles, and of peak levels of CO, O3, or SO2 appear to be less important. Traffic density is also consistently the most important environmental predictor in multiple-pollutant models, with combined relative risks up to about 1.2. However, from these findings it is not possible to discern which aspects of traffic (pollution, noise, stress) may be the most relevant to public health or whether an area-based predictor such as traffic density may have an inherent advantage over localized measures of ambient air quality. It is also possible that traffic density could be a marker for unmeasured pollutants or for geographic gradients per se. Pending resolution of these issues, including replication in other cohorts, it will be difficult to formulate additional cost-effective pollution control strategies that are likely to benefit public health.

Chronic obstructive pulmonary disease mortality in diesel-exposed railroad workers.

Diesel exhaust is a mixture of combustion gases and ultrafine particles coated with organic compounds. There is concern whether exposure can result in or worsen obstructive airway diseases, but there is only limited information to assess this risk. U.S. railroad workers have been exposed to diesel exhaust since diesel locomotives were introduced after World War II, and by 1959, 95% of the locomotives were diesel. We conducted a case-control study of railroad worker deaths between 1981 and 1982 using U.S. Railroad Retirement Board job records and next-of-kin smoking, residential, and vitamin use histories. There were 536 cases with chronic obstructive pulmonary disease (COPD) and 1,525 controls with causes of death not related to diesel exhaust or fine particle exposure. After adjustment for age, race, smoking, U.S. Census region of death, vitamin use, and total years off work, engineers and conductors with diesel-exhaust exposure from operating trains had an increased risk of COPD mortality. The odds of COPD mortality increased with years of work in these jobs, and those who had worked >/= 16 years as an engineer or conductor after 1959 had an odds ratio of 1.61 (95% confidence interval, 1.12-2.30) . These results suggest that diesel-exhaust exposure contributed to COPD mortality in these workers. Further study is needed to assess whether this risk is observed after exposure to exhaust from later-generation diesel engines with modern emission controls.

What's driving Twin Cities air quality?

Air quality affects the health of patients, particularly those with asthma, COPD, cardiovascular disease, and other heart problems. Epidemiological studies show that common air pollution may have health effects in sensitive populations even when the air quality is within Environmental Protection Agency standards. In Minnesota, the main 2 pollutants of concern are ozone and fine particles. Emissions from motor vehicles are a major source of each. This article discusses these pollutants and reports on the work of the Minnesota Pollution Control Agency in measuring air quality and alerting the public about air-quality problems.

Induction of sister chromatid exchanges in traffic policemen exposed to vehicular exhaust.

In urban areas there is an explosive growth of population and the number of automobiles. The ever-increasing vehicular traffic density is posing continued threat to the ambient air quality. Traffic policemen as a group of workers are exposed occupationally to the pollutants from vehicular exhaust. Sister chromatid exchanges (SCEs) as a biomarker of the pollutant's effect, were analyzed in peripheral blood lymphocytes of 85 traffic policemen and 60 control subjects. There was a significant increase in the mean SCEs+/-S.D./cell in the exposed group (9.31+/-5.29) when compared to the controls (4.18+/-1.85). Thus the present study concludes that vehicular exhaust might induce cytogenetic damage in traffic police. Further, the more pronounced frequency of SCEs observed in the smoking traffic policemen than in the non-smoking group suggests the joint effect of smoking and vehicular exhaust.

Responses of well-differentiated nasal epithelial cells exposed to particles: role of the epithelium in airway inflammation.

Numerous epidemiological studies support the contention that ambient air pollution particles can adversely affect human health. To explain the acute inflammatory process in airways exposed to particles, a number of in vitro studies have been performed on cells grown submerged on plastic and poorly differentiated, and on cell lines, the physiology of which is somewhat different from that of well-differentiated cells. In order to obtain results using a model system in which epithelial cells are similar to those of the human airway in vivo, apical membranes of well-differentiated human nasal epithelial (HNE) cells cultured in an air-liquid interface (ALI) were exposed for 24 h to diesel exhaust particles (DEP) and Paris urban air particles (PM(2.5)). DEP and PM(2.5) (10-80 microg/cm(2)) stimulated both IL-8 and amphiregulin (ligand of EGFR) secretion exclusively towards the basal compartment. In contrast, there was no IL-1beta secretion and only weak non-reproducible secretion of TNF-alpha. IL-6 and GM-CSF were consistently stimulated towards the apical compartment and only when cells were exposed to PM(2.5). ICAM-1 protein expression on cell surfaces remained low after particle exposure, although it increased after TNF-alpha treatment. Internalization of particles, which is believed to initiate oxidative stress and proinflammatory cytokine expression, was restricted to small nanoparticles (< or =40 nm). Production of reactive oxygen species (ROS) was detected, and DEP were more efficient than PM(2.5). Collectively, our results suggest that airway epithelial cells exposed to particles augment the local inflammatory response in the lung but cannot alone initiate a systemic inflammatory response.

[Carbon monoxide contamination: an environmental health problem]. / Contaminación por monóxido de carbono: un problema de salud ambiental.

Carbon monoxide is considered to be a major factor contaminating earth's atmosphere. The main sources producing this contamination are cars using gasoline or diesel fuel and industrial processes using carbon compounds; these two are responsible for 80% of carbon monoxide being emitted to the atmosphere. This substance has a well-known toxic effect on human beings and its acute poisonous effects (including death) have been widely studied; however, its long-term chronic effects are still not known. During the last few years, experimental research on animals and studies of human epidemiology have established the relationship between chronic exposure to low and middle levels of carbon monoxide in breathable air and adverse effects on human health, especially on organs consuming large amounts of oxygen such as the heart and brain. Harmful cardiovascular and neuropsychological effects have been documented in carbon monoxide concentration in air of less than 25 ppm and in carboxyhaemoglobin levels in blood of less than 10%. The main cardiac damage described to date has been high blood pressure, cardiac arrhythm and electrocardiograph signs of ischemia. Lack of memory, attention, concentration and Parkinson-type altered movement are the neuropsychological changes most frequently associated with chronic exposure to low levels of carbon monoxide and carboxyhaemoglobin.

Diesel exhaust particles enhance T-cell activation in severe asthmatics.

Prevalence of asthma is increasing in westernized countries. Epidemiological studies showed the impact of traffic pollution on the triggering of asthma symptoms and exacerbations, and this effect is mainly attributed to the polycyclic aromatic hydrocarbon core of diesel exhaust particles (DEP). However, although DEP induce IgE synthesis, little is known of their role on T-cell activation, the main cells orchestrating asthma inflammation. We assessed the effect of DEP on T-cell activation in severe uncontrolled asthmatics during (n = 13) and outside (n = 19) exacerbations. Results were compared with data obtained in healthy controls (n = 14). Peripheral blood mononuclear cells were cultured in the presence of low-dose DEP. T-cell activation markers, CD69 and CD25, interleukin-4 (IL-4) and interferon (IFN)-gamma production and T-cell proliferation were assessed by flow cytometry. DEP exposure increased the proportion of CD3+CD69+ T cells in all subjects. The proportion of CD25+ T cells increased under DEP stimulation in the exacerbation group only. IFN-gamma- and IL-4-producing T cells increased in both asthmatic groups, especially during exacerbations, but not in controls. This effect was more pronounced for IL-4. In response to DEP stimulation, T-cell proliferation increased in higher proportion in asthmatics compared with controls. These results show that DEP activate T cells in asthmatics only, with a higher effect during exacerbations. This is in keeping with epidemiological data which demonstrated that DEP trigger respiratory symptoms in asthmatics but not in controls. The higher effect of DEP in exacerbated asthmatics suggests that uncontrolled asthma is a risk factor for aggravation under exposure to traffic pollutants.

[Health significance of inhaled particles]. / Gesundheitliche Bedeutung inhalierter Stäube.

Particulates refer to particles, dust, dirt, soot and aerosol mists that has suspended in the surrounding air. They may consist of solids of various forms including fibres or liquids. Long term exposure to silicon dioxide containing dusts (crystalline silica: quartz, tridymite, cristobalite, coesite, stishovite) may cause pneumoconiosis in the form of acute or/either chronic silicosis. Asbestos refers to a divers family of crystalline hydrated fibrous siliates typically exhibiting a greater tha 3:1 length ot diameter ratio. It is subdivided into serpentine (Chrysotile) and amphibole (crocidolite, amosite, anthophyllite, tremolite, actinolite). Exposure to asbestos fibres may cause lung fibrosis and promote cancer of the lung or the pleura. Besides the induction of malignant diseases dust exposure may result in obstructive as well as restrictive lung diseases which may be compensate in case of the recognition as a occupational diseases. Other occupational exposures leading to pneumoconiosis are caused be talc, or metals including aluminium containing dusts. Also the group of man-made mineral (MMMFs) or vitreous fibres (MMVFs), including glass wool, rock wool, slag wool, glass filaments, microfibres, refractory ceramic fibres are bioactive under certain experimental conditions. Although it has been shown that MMMFs may cause malignancies when injected intraperitoneally in high quantities in rodents, inhalation trials and human studies could not reproduce these results in the same precision. Fine particles (particulate matter = PM) comprise one of the most widespread and harmful air pollutants in the industrialized world. PM may cause worsening of asthma and other respiratory diseases, reduce lung function development in children, potentially increased the risk of premature death in the elderly and enhance mortality from cardiac diseases. Because of the small size PM2.5 is seen to be even more hazardous than PM10.

Contaminación por monóxido de carbono: un problema de salud ambiental / Carbon monoxide contamination: an environmental health problem

El monóxido de carbono es considerado uno de los mayores contaminantes de la atmósfera terrestre. Sus principales fuentes productoras responsables de aproximadamente 80 por ciento de las emisiones, son los vehículos automotores que utilizan como combustible gasolina o diesel y los procesos industriales que utilizan compuestos del carbono. Esta sustancia es bien conocida por su toxicidad para el ser humano. Sus efectos tóxicos agudos incluida la muerte han sido estudiados ampliamente; sin embargo, sus potenciales efectos adversos a largo plazo son poco conocidos. En los últimos años, los estudios de investigación experimentales en animales y epidemiológicos en humanos han evidenciado relación entre población expuesta en forma crónica a niveles medios y bajos de monóxido de carbono en aire respirable y la aparición de efectos adversos en la salud humana especialmente en órganos de alto consumo de oxígeno como cerebro y corazón. Se han documentado efectos nocivos cardiovasculares y neuropsicológicos en presencia de concentraciones de monóxido de carbono en aire inferiores a 25 partes por millón y a niveles de carboxihemoglobina en sangre inferiores a 10 por ciento. Las alteraciones cardiovasculares que se han descrito son hipertensión arterial, aparición de arritmias y signos electrocardiográficos de isquemia. Déficit en memoria, atención, concentración y alteraciones del movimiento tipo parkinsonismo, son los cambios neuropsicológicos con mayor frecuencia asociados a exposición crónica a bajos niveles de monóxido de carbono y carboxihemoglobina.

Carbon monoxide is considered to be a major factor contaminating earths atmosphere. The main sources producing this contamination are cars using gasoline or diesel fuel and industrial processes using carbon compounds; these two are responsible for 80 percent of carbon monoxide being emitted to the atmosphere. This substance has a well-known toxic effect on human beings and its acute poisonous effects (including death) have been widely studied; however, its long-term chronic effects are still not known. During the last few years, experimental research on animals and studies of human epidemiology have established the relationship between chronic exposure to low and middle levels of carbon monoxide in breathable air and adverse effects on human health, especially on organs consuming large amounts of oxygen such as the heart and brain. Harmful cardiovascular and neuropsychological effects have been documented in carbon monoxide concentration in air of less than 25 ppm and in carboxyhaemoglobin levels in blood of less than 10 percent. The main cardiac damage described to date has been high blood pressure, cardiac arrhythm and electrocardiograph signs of ischemia. Lack of memory, attention, concentration and Parkinson-type altered movement are the neuropsychological changes most frequently associated with chronic exposure to low levels of carbon monoxide and carboxyhaemoglobin.

Policy and programmatic importance of spatial alignment of data sources.

Geographic information systems have proven instrumental in assessing environmental impacts on individual and community health, but numerous methodological challenges are associated with analyses of highly localized phenomena in which spatially misaligned data are used. In a case study based on child care facility and traffic data for the Los Angeles metropolitan area, we assessed the extent of facility misclassification with spatially unreconciled data from 3 different governmental agencies in an attempt to identify child care centers in which young children are at risk from high concentrations of toxic vehicle-exhaust pollutants. Relative to geographically corrected data, unreconciled information produced a modest bias in terms of aggregated number of facilities at risk and a substantial number of false positives and negatives.