Exposure to traffic and the onset of myocardial infarction.

BACKGROUND: An association between exposure to vehicular traffic in urban areas and the exacerbation of cardiovascular disease has been suggested in previous studies. This study was designed to assess whether exposure to traffic can trigger myocardial infarction. METHODS: We conducted a case-crossover study in which cases of myocardial infarction were identified with the use of data from the Cooperative Health Research in the Region of Augsburg Myocardial Infarction Registry in Augsburg, in southern Germany, for the period from February 1999 to July 2001. There were 691 subjects for whom the date and time of the myocardial infarction were known who had survived for at least 24 hours after the event, completed the registry's standardized interview, and provided information on factors that may have triggered the myocardial infarction. Data on subjects' activities during the four days preceding the onset of symptoms were collected with the use of patient diaries. RESULTS: An association was found between exposure to traffic and the onset of a myocardial infarction within one hour afterward (odds ratio, 2.92; 95 percent confidence interval, 2.22 to 3.83; P<0.001). The time the subjects spent in cars, on public transportation, or on motorcycles or bicycles was consistently linked with an increase in the risk of myocardial infarction. Adjusting for the level of exercise on a bicycle or for getting up in the morning changed the estimated effect of exposure to traffic only slightly (odds ratio for myocardial infarction, 2.73; 95 percent confidence interval, 2.06 to 3.61; P<0.001). The subject's use of a car was the most common source of exposure to traffic; nevertheless, there was also an association between time spent on public transportation and the onset of a myocardial infarction one hour later. CONCLUSIONS: Transient exposure to traffic may increase the risk of myocardial infarction in susceptible persons.

Localization, release and bioavailability of pollen allergens: the influence of environmental factors.

Allergens are integral constituents of plants or animals and their normal functions and localization are being characterized. To trigger responses in humans, allergens must become bioavailable and the role of air pollutants--for example diesel-exhaust particles --in this process is causing concern. Finally, the fact that some pollen releases eicosanoid-like proinflammatory mediators may have wide implications.

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.

Application of a geographic information system to explore associations between air pollution and micronucleus frequencies in African American children and adults.

Exposure to air pollution has been associated with adverse respiratory and cardiovascular health outcomes in both children and adults. In this study, we used geographic information systems (GISs) to explore possible associations between chromosomal damage in 65 African American children and their mothers from Oakland, California, and both proximity to traffic and regional ozone levels. Study participants were interviewed at the Healthy Child Clinic of Children's Hospital, Oakland, and their blood and buccal cells were collected for assessment of chromosomal damage by the micronucleus (MN) assay. Regional ozone levels, which decreased from April to November with a secondary peak in late summer, were highly correlated with season by month (r=-0.84, P=0.02) and strongly associated with MN frequency (frequency ratio (FR): 3.37, 95% confidence interval (CI): 1.30-8.72) in both cell types of children and adults. Additionally, MN frequencies were modestly associated with individual measures of traffic density in children (FR=2.45, 95% CI=0.86-7.10), but not in adults; this suggests a greater vulnerability to traffic-related air pollution in children. Smoking in the household also increased MN frequency in the lymphocytes of children (FR: 1.13, 95%CI: 1.01-1.24) and adults (FR: 1.06, 95%CI: 0.99-1.13), whereas vitamin use in adults decreased MN frequency in both lymphocytes and buccal cells (FR: 0.17, 95%CI: 0.02-1.31; FR: 0.18, 95%CI: 0.03-1.18, respectively). Our data indicate that GIS-generated measures of traffic density for individual households augment regional ozone monitoring data used to assess effects of air pollution. This approach helped to demonstrate elevated cytogenetic damage in exposed minority children.

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.

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.

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.

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.

Scale and causes of lead contamination in Chinese tea.

We investigated the scale and causes of Pb contamination in Chinese tea. Lead concentrations in 1,225 tea samples collected nationally between 1999 and 2001 varied from <0.2 to 97.9 mg kg(-1) dry weight (DW), with 32% of the samples exceeding the national maximum permissible concentration (MPC) of 2.0 mg kg(-1) DW and a significant difference between tea types. There was an increasing trend in tea Pb concentration from 1989 to 2000. Proximity to highway and surface dust contamination were found to cause elevated Pb concentrations in tea leaves. Furthermore, Pb concentration in tea leaves correlated significantly and positively with soil extractable Pb, and negatively with soil pH, suggesting that root uptake of Pb from soils also contributed to Pb accumulation in tea. Potential contributions to human Pb intake from drinking tea were small at the median or national MPC Pb values, but considerable at the highest concentration found in the study.

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.

[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.

[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.

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.

Diesel exhaust particles in lung acutely enhance experimental peripheral thrombosis.

BACKGROUND: Pollution by particulates has consistently been associated with increased cardiovascular morbidity and mortality, but a plausible biological basis for this association is lacking. METHODS AND RESULTS: Diesel exhaust particles (DEPs) were instilled into the trachea of hamsters, and blood platelet activation, experimental thrombosis, and lung inflammation were studied. Doses of 5 to 500 micro g of DEPs per animal induced neutrophil influx into the bronchoalveolar lavage fluid with elevation of protein and histamine but without lactate dehydrogenase release. The same doses enhanced experimental arterial and venous platelet rich-thrombus formation in vivo. Blood samples taken from hamsters 30 and 60 minutes after instillation of 50 micro g of DEPs yielded accelerated aperture closure (ie, platelet activation) ex vivo, when analyzed in the Platelet Function Analyser (PFA-100). The direct addition of as little as 0.5 micro g/mL DEPs to untreated hamster blood significantly shortened closure time in vitro. CONCLUSIONS: The intratracheal instillation of DEPs leads to lung inflammation as well as a rapid activation of circulating blood platelets. The kinetics of platelet activation are consistent with the reported clinical occurrence of thrombotic complications after exposure to pollutants. Our findings, therefore, provide a plausible explanation for the increase in cardiovascular morbidity and mortality accompanying urban air pollution.

Effect of glutathione-S-transferase M1 and P1 genotypes on xenobiotic enhancement of allergic responses: randomised, placebo-controlled crossover study.

BACKGROUND: Particulate pollution is associated with the occurrence of asthma and allergy. The model pollutant, diesel exhaust particles, can participate with allergens in starting and exacerbating allergic airway diseases in part by production of reactive oxygen species. Glutathione-S-transferases (GSTs) can metabolise reactive oxygen species and detoxify xenobiotics present in diesel exhaust particles. We tested the hypothesis that null genotypes for GSTM1 and GSTT1, and GSTP1 codon 105 variants (I105 and V105) are key regulators of the adjuvant effects of diesel exhaust particles on allergic responses. METHODS: Patients sensitive to the ragweed allergen were challenged intranasally with allergen alone and with allergen plus diesel exhaust particles in a randomised order at separate visits. Nasal allergen-specific IgE, histamine, interleukin 4, and interferon gamma concentrations were measured before and 24 h after challenge. FINDINGS: Individuals with GSTM1 null or the GSTP1 I105 wildtype genotypes showed enhanced nasal allergic responses in the presence of diesel exhaust particles. Compared with patients with a functional GSTM1 genotype, GSTM1 null patients had a significantly larger increase in IgE (median 102.5 U/mL [range 1.0-510.5] vs 45.5 U/mL [1.5-60.6], p=0.03) and histamine (14.0 nmol/L [-0.2-24.7] vs 7.4 nmol/L [1.2-12.3], p=0.02) after diesel exhaust particles plus allergen challenge. The I105 GSTP1 genotype was associated with an increase in IgE (120.3 U/mL [6.7-510.5] vs 27.7 U/mL [-1.5-60.6], p=0.03) and histamine (13.8 nmol/L [3.1-24.7] vs 5.2 nmol/L [-0.2-19.6], p=0.01) after challenge with diesel exhaust particles and allergens. The diesel exhaust particles enhancement was largest in patients with both the GSTM1 null and GSTP1 I/I genotypes. INTERPRETATION: GSTM1 and GSTP1 modify the adjuvant effect of diesel exhaust particles on allergic inflammation.

Time course of gene expression of inflammatory mediators in rat lung after diesel exhaust particle exposure.

Diesel exhaust particles (DEPs) at three concentrations (5, 35, and 50 mg/kg body weight) were instilled into rats intratracheally. We studied gene expression at 1, 7, and 30 days postexposure in cells obtained by bronchoalveolar lavage (BAL) and in lung tissue. Using real-time reverse transcriptase-polymerase chain reaction (RT-PCR), we measured the mRNA levels of eight genes [interleukin (IL)-1beta, IL-6, IL-10, iNOS (inducible nitric oxide synthase), MCP-1 (monocyte chemoattractant protein-1), MIP-2 (macrophage inflammatory protein-2), TGF-beta1 (transforming growth factor-beta1), and TNF-alpha (tumor necrosis factor-alpha )] in BAL cells and four genes [IL-6, ICAM-1 (intercellular adhesion molecule-1), GM-CSF (granulocyte/macrophage-colony stimulating factor), and RANTES (regulated upon activation normal T cell expressed and secreted)] in lung tissue. In BAL cells on day 1, high-dose exposure induced a significant up-regulation of IL-1beta, iNOS, MCP-1, and MIP-2 but no change in IL-6, IL-10, TGF-beta1, and TNF-alpha mRNA levels. There was no change in the mRNA levels of IL-6, RANTES, ICAM-1, and GM-CSF in lung tissue. Nitric oxide production and levels of MCP-1 and MIP-2 were increased in the 24-hr culture media of alveolar macrophages (AMs) obtained on day 1. IL-6, MCP-1, and MIP-2 levels were also elevated in the BAL fluid. BAL fluid also showed increases in albumin and lactate dehydrogenase. The cellular content in BAL fluid increased at all doses and at all time periods, mainly due to an increase in polymorphonuclear leukocytes. In vitro studies in AMs and cultured lung fibroblasts showed that lung fibroblasts are a significant source of IL-6 and MCP-1 in the lung.

Air pollution and ST-segment depression in elderly subjects.

Increased levels of daily ambient particle pollution have been associated with increased risk of cardiovascular morbidity. Black carbon (BC) is a measure of the traffic-related component of particles. We investigated associations between ambient pollution and ST-segment levels in a repeated-measures study including 269 observations on 24 active Boston residents 61-88 years of age, each observed up to 12 times from June through September 1999. The protocol involved continuous Holter electrocardiogram monitoring including 5 min of rest, 5 min of standing, 5 min of exercise outdoors, 5 min of recovery, and 20 cycles of paced breathing. Pollution-associated ST-depression was estimated for a 10th- to 90th-percentile change in BC. We calculated the average ST-segment level, referenced to the P-R isoelectric values, for each portion of the protocol. The mean BC level in the previous 12 hr, and the BC level 5 hr before testing, predicted ST-segment depression in most portions of the protocol, but the effect was strongest in the postexercise periods. During postexercise rest, an elevated BC level was associated with -0.1 mm ST-segment depression (p = 0.02 for 12-hr mean BC; p = 0.001 for 5-hr BC) in continuous models. Elevated BC also predicted increased risk of ST-segment depression > or = 0.5 mm among those with at least one episode of that level of ST-segment depression. Carbon monoxide was not a confounder of this association. ST-segment depression, possibly representing myocardial ischemia or inflammation, is associated with increased exposure to particles whose predominant source is traffic.

Local variations in CO and particulate air pollution and adverse birth outcomes in Los Angeles County, California, USA.

We extended our previous analyses of term low birth weight (LBW) and preterm birth to 1994-2000, a period of declining air pollution levels in the South Coast Air Basin. We speculated that the effects we observed previously for carbon monoxide, particulate matter < 10 microm in aerodynamic diameter (PM10), and traffic density were attributable to toxins sorbed to primary exhaust particles. Focusing on CO, PM10, and particulate matter < 2.5 microm in aerodynamic diameter (PM2.5), we examined whether varying residential distances from monitoring stations affected risk estimates, because effect attenuation may result from local pollutant heterogeneity inadequately captured by ambient stations. We geocoded home locations, calculated the distance to the nearest air monitors, estimated exposure levels by pregnancy period, and performed logistic regression analyses for subjects living within 1-4 mi of a station. For women residing within a 1-mi distance, we observed a 27% increase in risk for high (> or = 75th percentile) first-trimester CO exposures and preterm birth and a 36% increase for high third-trimester pregnancy CO exposures and term LBW. For particles, we observed similar size effects during early and late pregnancy for both term LBW and preterm birth. In contrast, smaller or no effects were observed beyond a 1-mi distance of a residence from a station. Associations between CO and PM10 averaged over the whole pregnancy and term LBW were generally smaller than effects for early and late pregnancy. These new results for 1994-2000 generally confirm our previous observations for the period 1989-1993, again linking CO and particle exposures to term LBW and preterm birth. In addition, they confirm our suspicions about having to address local heterogeneity for these pollutants in Los Angeles.

Composition, toxicity, and mutagenicity of particulate and semivolatile emissions from heavy-duty compressed natural gas-powered vehicles.

Particulate matter (PM) and vapor-phase semivolatile organic compounds (SVOC) were collected from three buses fueled by compressed natural gas. The bus engines included a well-functioning, conventional engine; a "high emitter" engine; and a new technology engine with an oxidation catalyst. Chemical analysis of the emissions showed differences among these samples, with the high emitter sample containing markers of engine oil constituents. PM + SVOC samples were also collected for mutagenicity and toxicity testing. Extraction efficiencies from the collection media were lower than for similarly collected samples from gasoline or diesel vehicles. Responses to the recovered samples were compared on the basis of exhaust volume, to incorporate the emission rates into the potency factors. Mutagenicity was assessed by Salmonella reverse mutation assay. Mutagenicity was greatest for the high emitter sample and lowest for the new technology sample. Metabolic activation reduced mutagenicity in strain TA100, but not TA98. Toxicity, including inflammation, cytotoxicity, and parenchymal changes, was assessed 24 h after intratracheal instillation into rat lungs. Lung responses were generally mild, with little difference between the responses to equivalent volumes of emissions from the normal emitter and the new technology, but greater responses for the high emitter. These emission sample potencies are further compared on the basis of recovered mass with previously reported samples from normal and high-emitter gasoline and diesel vehicles. While mutagenic potencies for the CNG emission samples were similar to the range observed in the gasoline and diesel emission samples, lung toxicity potency factors were generally lower than those for the gasoline and diesel samples.

Carbon monoxide poisoning from portable electric generators.

BACKGROUND: While the overall death rate from unintentional carbon monoxide (CO) poisoning has decreased in the United States due to improved automobile emissions controls and a decline in CO poisonings from motor vehicles, exposures have not changed from some sources of CO. One of these is the operation of portable electrical generators in poorly ventilated spaces. This study sought to describe the population poisoned from CO produced by portable electric generators, and to determine the reasons that generators are operated in a hazardous fashion. METHODS: Cases of CO poisoning referred for treatment with hyperbaric oxygen at Virginia Mason Medical Center in Seattle from November 1978 to March 2004 were reviewed. Those cases that resulted from portable generator use were selected for analysis. RESULTS: Sixty-three patients aged 2 to 85 years were treated for CO poisoning from portable electric generators. They included 34 males and 29 females who were poisoned in 37 separate incidents. Thirty-four lost consciousness with the exposure. Of the 63 total patients, 60 spoke English. Generators were typically used when normal electrical service was disrupted by a storm or in remote locations. In 29 of 37 incidents, the generator was operated in the home environment, most commonly in the garage. Lack of awareness of the dangers of CO poisoning or lack of knowledge of ventilation requirements were the most commonly identified reasons. CONCLUSIONS: CO poisoning from portable electric generators occurs in a characteristic population, in a few typical locations and for a limited number of reasons. This information may help target prevention efforts for this form of poisoning, such as warning labels or educational programs.