Abstract  BACKGROUND: Growing evidence indicates that ambient air pollution is associated with exacerbation of chronic diseases like chronic pulmonary disease. A prospective panel study was conducted to investigate short-term changes of blood markers of inflammation and coagulation in response to daily changes in air pollution in Erfurt, Germany. 12 clinical visits were scheduled and blood parameters were measured in 38 male patients with chronic pulmonary disease during winter 2001/2002. Additive mixed models with random patient intercept were applied, adjusting for trend, weekday, and meteorological parameters. Hourly data on ultrafine particles (UFP, 0.01-0.1 mum), accumulation mode particles (ACP, 0.1-1.0 mum), PM10 (particulate matter <10 mum in diameter), elemental (EC) and organic carbon (OC), gaseous pollutants (nitrogen monoxide [NO], nitrogen dioxide [NO2], carbon monoxide [CO], and sulphur dioxide [SO2]) were collected at a central monitoring site and meteorological data were received from an official network. For each person and visit the individual 24-hour average of pollutants immediately preceding the blood withdrawal (lag 0) up to day 5 (lag1-4) and 5-day running means were calculated. RESULTS: Increased levels of fibrinogen were observed for an increase in one interquartile range of UFP, PM10, EC, OC, CO, and NO revealing the strongest effect for lag 3. E-selectin increased in association with ACP and PM10 with a delay of one day. The ACP effect was also seen with the 5-day-mean. The pattern found for D-dimer was inconsistent. Prothrombin fragment 1+2 decreased with lag 4 consistently for all particulate pollutants. Von Willebrand factor antigen (vWF) showed a consistent decrease in association with almost all air pollutants with all lags except for lag 0. No associations were found for C-reactive protein, soluble intercellular adhesion molecule 1, serum amyloid A and factor VII. CONCLUSION: These results suggest that elevated concentrations of air pollution are associated with changes in some blood markers of inflammation and coagulation in patients with chronic pulmonary disease. The clinical implications of these findings need further investigation.

Abstract  Biomass burning represents an important source of atmospheric aerosols and greenhouse gases, yet little is known about its interannual variability or the underlying mechanisms regulating this variability at continental to global scales. Here we investigated fire emissions during the 8 year period from 1997 to 2004 using satellite data and the CASA biogeochemical model. Burned area from 2001–2004 was derived using newly available active fire and 500 m. burned area datasets from MODIS following the approach described by Giglio et al. (2006). ATSR and VIRS satellite data were used to extend the burned area time series back in time through 1997. In our analysis we estimated fuel loads, including organic soil layer and peatland fuels, and the net flux from terrestrial ecosystems as the balance between net primary production (NPP), heterotrophic respiration (Rh), and biomass burning, using time varying inputs of precipitation (PPT), temperature, solar radiation, and satellite-derived fractional absorbed photosynthetically active radiation (fAPAR). For the 1997–2004 period, we found that on average approximately 58 Pg C year−1 was fixed by plants as NPP, and approximately 95% of this was returned back to the atmosphere via Rh. Another 4%, or 2.5 Pg C year−1 was emitted by biomass burning; the remainder consisted of losses from fuel wood collection and subsequent burning. At a global scale, burned area and total fire emissions were largely decoupled from year to year. Total carbon emissions tracked burning in forested areas (including deforestation fires in the tropics), whereas burned area was largely controlled by savanna fires that responded to different environmental and human factors. Biomass burning emissions showed large interannual variability with a range of more than 1 Pg C year−1, with a maximum in 1998 (3.2 Pg C year−1) and a minimum in 2000 (2.0 Pg C year−1).

Abstract  We examined the associations between gaseous pollutants and hospitalization for chronic obstructive pulmonary diseases (COPD) among elderly people living in Vancouver, British Columbia, Canada, a city in which ambient air pollution levels are relatively low. We regressed the logarithm of daily counts of acute COPD hospitalization during the 5-year period from 1994 to 1998 on the daily mean levels of each pollutant, after accounting for seasonal and subseasonal fluctuations, non-Poisson dispersion, and weather variables. Nitrogen dioxide and carbon monoxide were significantly associated with hospitalization for COPD, and the magnitude of effects was increased slightly with increasing days of exposure averaging, with the relative risk for a 7-day average being 1.11 (95%CI: 1.04, 1.20) and 1.08 (1.02, 1.13) for nitrogen dioxide and carbon monoxide, respectively. There was no significant association between either sulfur dioxide or ozone and COPD hospitalization. The combined relative risk for all four gaseous pollutants on COPD hospitalization was 1.21. The effects of gaseous pollutants on COPD hospitalization were not significant after adjustment for PM10, although its inclusion did not have a marked effect on the point estimates for relative risks. Nitrogen dioxide has a significant impact on COPD hospitalization. Further studies are needed to separate the effects of single pollutants from the combined effects of the complex mixture of air pollutants in urban atmospheres.

Abstract  Two studies at three sites in the UK provided confirmation that systematic positive bias in NO2 diffusion tube measurement occurred because of changes to "within-tube" chemistry, rather than eddy diffusion at the mouth of the tube. In the first study in Cambridge, UK, sampler overestimation for 1 and 2 week exposures was compared to corresponding time-averaged monitor measurements (NO-NO2-NOx, O3) and weather variables. Noninearity between sampler and monitor NO2 measurements was interpreted in terms of spatial and temporal variations in relative and absolute availability of NO, NO2 and O3 at the site. A maximum overestimation occurred for an exposure mean NO2/NOx approximately 0.5. The separate contributions of reduced NO2 photolysis and eddy diffusion were compared in Study II using samplers of two materials, acrylic and quartz, and of different lengths (40, 55, 71 and 120 mm) at three sites: Norwich background, Cambridge intermediate, London kerbside. For compared sites, NO2 measured by acrylic samplers was significantly higher than for equivalent quartz samplers. For quartz samplers [NO2]mean was only just above the monitor at Norwich and London; sampler/monitor NO2 = 1.04 (P = 0.59) and 1.01(P = 0.76), respectively. For acrylic samplers the order of [NO2]mean was 40 mm > 120 mm > 71 mm > or = 55 mm. Excepting 40 mm samplers, this accords with a chemical bias where co-diffusing NO and 03 molecules in longer tubes have more time to react to form excess NO2. Bias in 40 mm samplers is discussed. Eddy diffusion is negligible for standard samplers because [NO2]mean was equivalent for 55 mm and 71 mm acrylic samplers and close to monitor NO2 for 71 mm quartz tubes. Both studies showed that sampler accuracy was dependent on location. Significantly, overestimation was greatest (approximately 3-4 ppb) where the NO2 annual mean was approximately 20 ppb, close to the UK and EU air quality standard of 21 ppb.

Abstract  BACKGROUND: The Democratic National Convention (DNC) in Boston, Massachusetts in 2004 provided an opportunity to evaluate the impacts of a localized and short-term but potentially significant change in traffic patterns on air quality, and to determine the optimal monitoring approach to address events of this nature. It was anticipated that the road closures associated with the DNC would both influence the overall air pollution level and the distribution of concentrations across the city, through shifts in traffic patterns. METHODS: To capture these effects, we placed passive nitrogen dioxide badges at 40 sites around metropolitan Boston before, during, and after the DNC, with the goal of capturing the array of hypothesized impacts. In addition, we continuously measured elemental carbon at three sites, and gathered continuous air pollution data from US EPA fixed-site monitors and traffic count data from the Massachusetts Highway Department. RESULTS: There were significant reductions in traffic volume on the highway with closures north of Boston, with relatively little change along other highways, indicating a more isolated traffic reduction rather than an across-the-board decrease. For our nitrogen dioxide samples, while there was a relatively small change in mean concentrations, there was significant heterogeneity across sites, which corresponded with our a priori classifications of road segments. The median ratio of nitrogen dioxide concentrations during the DNC relative to non-DNC sampling periods was 0.58 at sites with hypothesized traffic reductions, versus 0.88 for sites with no changes hypothesized and 1.15 for sites with hypothesized traffic increases. Continuous monitors measured slightly lower concentrations of elemental carbon and nitrogen dioxide during road closure periods at monitors proximate to closed highway segments, but not for PM2.5 or further from major highways. CONCLUSION: We conclude that there was a small but measurable influence of DNC-related road closures on air quality patterns in the Boston area, and that a low-cost monitoring study combining passive badges for spatial heterogeneity and continuous monitors for temporal heterogeneity can provide useful insight for community air quality assessments.

Abstract  Multipollutant models are frequently used to differentiate roles of multiple pollutants in epidemiologic studies of ambient air pollution. In the presence of differing levels of measurement error across pollutants under consideration, however, they can be biased and as misleading as single-pollutant models. Their appropriate interpretation depends on the relationships among the pollutant measurements and the outcomes in question. In situations where two or more pollutant variables may be acting as surrogates for the etiologic agent(s), multipollutant models can help identify the best surrogate, but the risk estimates may be influenced by inclusion of a second variable that is not itself an independent risk factor for the outcome in question. In this paper, these issues will be illustrated in the context of an ongoing study of emergency visits in Atlanta. Emergency department visits from 41 of 42 hospitals serving the twenty-county Atlanta metropolitan area for the period 1993-2004 (n=10,206,389 visits) were studied in relation to ambient pollutant levels, including speciated particle measurements from an intensive monitoring campaign at a downtown station starting in 1998. Relative to our earlier publications, reporting results through 2000, the period for which the speciated data are now available is now tripled (six years in length). Poisson generalized linear models were used to examine outcome counts in relation to three-day moving average concentrations of pollutants of a priori interest (ozone, nitrogen dioxide, carbon monoxide, sulfur dioxide, oxygenated hydrocarbons, PM10, coarse PM, PM2.5, and the following components of PM2.5: elemental carbon, organic carbon, sulfate, water-soluble transition metals.) In the present analysis, we report results for two outcome groups: a respiratory outcomes group and a cardiovascular outcomes group. For cardiovascular visits, associations were observed with CO, 3 NO2, and PM2.5 elemental carbon and organic carbon. In multipollutant models, CO was the strongest predictor. For respiratory visits, associations were observed with ozone, PM10, CO and NO2 in single-pollutant models. In multipollutant models, PM10 and ozone persisted as predictors, with ozone the stronger predictor. Caveats and considerations in interpreting the multipollutant model results are discussed.

Abstract  BACKGROUND: Consistent evidence has indicated that air pollution increases the risk of cardiovascular diseases. The underlying mechanisms linking air pollutants to increased cardiovascular risk are unclear. OBJECTIVES: We investigated the association between the pollution levels and changes in such global coagulation tests as the prothrombin time (PT) and the activated partial thromboplastin time (APTT) in 1218 normal subjects from the Lombardia Region, Italy. Plasma fibrinogen and naturally occurring anticoagulant proteins were also evaluated. METHODS: Hourly concentrations of particulate (PM10) and gaseous pollutants (CO, NO2, SO2, and O3) were obtained from 53 monitoring sites covering the study area. Generalized additive models were applied to compute standardized regression coefficients controlled for age, gender, body mass index, smoking, alcohol, hormone use, temperature, day of the year, and long-term trends. RESULTS: The PT became shorter with higher ambient air concentrations at the time of the study of PM10 (coefficient = -0.06; P < 0.05), CO (coefficient = -0.11; P < 0.001) and NO2 (coefficient =-0.06; P < 0.05). In the 30 days before blood sampling, the PT was also negatively associated with the average PM10 (coefficient = -0.08; P < 0.05) and NO2 (coefficient = -0.08; P < 0.05). No association was found between the APTT and air pollutant levels. In addition, no consistent relations with air pollution were found for fibrinogen, antithrombin, protein C and protein S. CONCLUSIONS: This investigation shows that air pollution is associated with changes in the global coagulation function, suggesting a tendency towards hypercoagulability after short-term exposure to air pollution. Whether these changes contribute to trigger cardiovascular events remains to be established.

Abstract  Nitrous acid is a significant photochemical precursor of the hydroxyl radical the key oxidant in the degradation of most air pollutants in the troposphere. The sources of nitrous acid in the troposphere, however, are still poorly understood. Recent atmospheric measurements revealed a strongly enhanced formation of nitrous acid during daytime via unknown mechanisms. Here we expose humic acid films to nitrogen dioxide in an irradiated tubular gas flow reactor and find that reduction of nitrogen dioxide on light-activated humic acids is an important source of gaseous nitrous acid. Our findings indicate that soil and other surfaces containing humic acid exhibit an organic surface photochemistry that produces reductive surface species, which react selectively with nitrogen dioxide. The observed rate of nitrous acid formation could explain the recently observed high daytime concentrations of nitrous acid in the boundary layer, the photolysis of which accounts for up to 60 per cent of the integrated hydroxyl radical source strengths. We suggest that this photo-induced nitrous acid production on humic acid could have a potentially significant impact on the chemistry of the lowermost troposphere.

Abstract  Nitrogen oxides are trace gases that critically affect atmospheric chemistry and aerosol formation1. Vegetation is usually regarded as a sink for these gases, although nitric oxide and nitrogen dioxide have been detected as natural emissions from plants2, 3. Here we use in situ measurements to show that solar ultraviolet radiation induces the emission of nitrogen oxide radicals (NOx) from Scots pine (Pinus sylvestris) shoots when ambient concentrations drop below one part per billion. Although this contribution is insignificant on a local scale, our findings suggest that global NOx emissions from boreal coniferous forests may be comparable to those produced by worldwide industrial and traffic sources.

Abstract  Background: Acute myocardial infarction (AMI) is the leading cause of death attributed to cardiovascular diseases. An association between traffic-related air pollution and AMI has been suggested, but the evidence is still limited. Objectives: to evaluate in a multi-centre study association between hospitalisation for first AMI and daily levels of traffic-related air pollution. Methods: We collected data on first AMI hospitalisations in 5 European cities. AMI registers were available in Augsburg and Barcelona; hospital discharge registers (HDRs) were used in Helsinki, Rome and Stockholm. NO2, CO and PM10 (particles <10 mu m) were measured at central monitoring sites. Particle number concentration (PNC), a proxy for ultrafine particles (<0.1 mu m), was measured for a year in each centre, and then modelled retrospectively for the whole study period. We used generalized additive models for statistical analyses. Age and 28-day fatality and season were considered as potential effect modifiers in the 3 HDR centres. Results: Nearly 27 000 cases of first AMI were recorded. There was a suggestion of an association of the same day CO and PNC levels with AMI: RR=1.005 (95% confidence interval: 1.000-1.010) per 0.2 mg/m3 and RR=1.005 (95%CI: 0.996-1.015) per 10000 particles/cm3, respectively. However, associations were only observed in the 3 cities with HDR, where power for city-specific analyses was higher. We observed in these cities the most consistent associations among fatal cases aged <75 years: RR at 1-day lag for CO=1.021 (95%CI: 1.000-1.048) per 0.2 mg/m3, for PNC= 1.058 (95% CI: 1.012-1.107) per 10000 particles/cm3, and for NO2=1.032 (95%CI: 0.998-1.066) per 8 mu g/m3. Effects of air pollution were more pronounced during the warm than the cold season. Conclusions: We found support for the hypothesis that exposure to traffic-related air pollution increases the risk of AMI. Most consistent associations were observed among fatal cases aged <75 years and in the warm season.

Abstract  #BACKGROUND: Cohort studies have reported increased risks of cardiopulmonary mortality from long-term air pollution exposure, but the evidence is limited and inconclusive. We studied the association between long-term exposure to source-specific air pollution and myocardial infarction (MI) in a case-control study of first-time MI cases and population controls age 45 to 70 years in Stockholm county in 1992 to 1994. METHODS: Home addresses during several decades were combined with historical emission databases and dispersion models to obtain annual mean levels of pollutants from traffic and heating during 30 years for 1397 cases and 1870 controls. Nitrogen dioxide (NO2), carbon monoxide (CO), and particulate matter with an aerodynamic diameter less than 10 microm (PM10) were used as indicators of traffic emissions and sulfur dioxide (SO2) as an indicator of emissions from residential heating. RESULTS: There was no association between long-term average air pollution exposure and overall MI, but an increased risk of fatal MI was suggested, especially for out-of-hospital death. After adjustment for cardiovascular risk factors, the odds ratio for fatal MI associated with a 5th to 95th percentile difference in 30-year average exposure was 1.51 (95% confidence interval = 0.96-2.16) for NO2, 1.22 (0.98-1.52) for CO, 1.39 (0.94-2.07) for PM10, and 1.24 (0.77-2.02) for SO2. For out-of-hospital death, the odds ratio related to NO2 exposure was 2.17 (1.05-4.51). CONCLUSIONS: This study provides some support for an association between long-term air pollution exposure and fatal cardiovascular disease.

Abstract  Objective: It is still unknown whether specific components in fine particles are associated with heart rate variability (HRV) reduction. Methods: We recruited 46 patients with or at risk for cardiovascular diseases to measure 24-hour HRV by ambulatory electrocardiographic monitoring. Fixed-site air-monitoring stations were used to represent participants' exposures to particles with aerodynamic diameters less than 10 ?m (PM10) and 2.5 ?m (PM2.5), and particulate components of sulfate, nitrate, organic carbon (OC) and elemental carbon, and gaseous pollutants. Results: We found that HRV reduction was associated with sulfate, OC, and PM2. 5 but not with the other five pollutants in single-pollutant models. Sulfate was found to remain in significant association with HRV reduction adjusting for OC and PM2.5 in three-pollutant models. Conclusions: Exposures to sulfate and OC in PM2.5were associated with HRV reduction in patients with or at risk for cardiovascular diseases.

Abstract  Objective: The authors conducted an investigation of the association between air pollution and arrhythmia. Methods: A prospective panel study (October 2000-April 2001) was conducted in Erfurt, Germany. Fifty-seven men with coronary heart disease were subjected to six 24-hour electrocardiogram recordings. Runs of supraventricular and ventricular tachycardia were associated with continuous ultrafine particle counts (UFP), accumulation mode particle counts (ACP), PM2,5, and gaseous pollutants. Poisson and linear regression models were applied adjusting for trend, weekday, and meteorologic data. Results: Elevated concentrations of UFP, ACP, PM2,5, and nitrogen dioxide increased the risk for supraventricular runs and the number of ventricular runs at almost all lags. Statistically significant associations were found predominantly in the previous 24 to 71 hours and with the 5-day moving average. Conclusion: Elevated concentrations of fine and ultrafine particle increased the risk of arrhythmia in men with coronary heart disease.

Abstract  The National Children's Study is considering a wide spectrum of airborne pollutants that are hypothesized to potentially influence pregnancy outcomes, neurodevelopment, asthma, atopy, immune development, obesity, and pubertal development. In this article we summarize six applicable exposure assessment lessons learned from the Centers for Children's Environmental Health and Disease Prevention Research that may enhance the National Children's Study: a) Selecting individual study subjects with a wide range of pollution exposure profiles maximizes spatial-scale exposure contrasts for key pollutants of study interest. b) In studies with large sample sizes, long duration, and diverse outcomes and exposures, exposure assessment efforts should rely on modeling to provide estimates for the entire cohort, supported by subject-derived questionnaire data. c) Assessment of some exposures of interest requires individual measurements of exposures using snapshots of personal and microenvironmental exposures over short periods and/or in selected microenvironments. d) Understanding issues of spatial-temporal correlations of air pollutants, the surrogacy of specific pollutants for components of the complex mixture, and the exposure misclassification inherent in exposure estimates is critical in analysis and interpretation. e) "Usual" temporal, spatial, and physical patterns of activity can be used as modifiers of the exposure/outcome relationships. f) Biomarkers of exposure are useful for evaluation of specific exposures that have multiple routes of exposure. If these lessons are applied, the National Children's Study offers a unique opportunity to assess the adverse effects of air pollution on interrelated health outcomes during the critical early life period.

Abstract  The report provides the Oversight Review Board`s (ORB`s) conclusions on the performance of the National Acid Precipitation Assessment Program (NAPAP) as requested by the Joint Chairs Council, and suggests lessons to be drawn from the NAPAP experience which may be of use in other similar endeavors.The ORB concludes that, taken as a whole, NAPAP was a successful enterprise which furthered effective decision making with respect to acid precipitation and other air quality matters, which improved scientific and technical understanding of underlying processes, and which provided an innovative institutional departure for addressing other problems at the intersection of science, technology and policy.

Abstract  To clarify the health effects of ozone exposure in young children, the authors studied the association between air pollution and hospital admissions for acute respiratory problems in children less than 2 years of age during the 15-year period from 1980 to 1994 in Toronto, Canada. The daily time series of admissions was adjusted for the influences of day of the week, season, and weather. A 35% (95% confidence interval: 19%, 52%) increase in the daily hospitalization rate for respiratory problems was associated with a 5-day moving average of the daily 1-hour maximum ozone concentration of 45 parts per billion, the May-August average value. The ozone effect persisted after adjustment for other ambient air pollutants or weather variables. Ozone was not associated with hospital admissions during the September-April period. Ambient ozone levels in the summertime should be considered a risk factor for respiratory problems in children less than 2 years of age.

Abstract  BACKGROUND: The mechanism behind the triggering effect of fine particulate matter (PM) air pollution on cardiovascular events remains elusive. We postulated that elevated levels of PM would be associated with increased blood levels of inflammatory and thrombotic markers in elderly individuals. We also hypothesized that elevated PM would increase levels of cytokines in individuals with heart disease. METHODS: We measured these blood markers in 47 elderly individuals with (23) and without (16 COPD and 8 healthy) cardiovascular disease (CVD) on 2 or 3 mornings over a 5 or 10-day period between February 2000 and March 2002. Blood measures were paired with residence level outdoor PM measured by nephelometry. Analyses determined the within-individual effect of 24-hour averaged outdoor PM on blood measures. RESULTS: Analyses found no statistically significant effect of a same day 10 ug/m3 increase in fine PM on log transformed levels of CRP 1.21 fold-rise [95% CI: 0.86, 1.70], fibrinogen 1.02 fold-rise [95% CI: 0.98, 1.06], or D-dimer 1.02 fold-rise [95% CI: 0.88, 1.17] in individuals with CVD. One-day lagged analyses in the CVD subgroup found similar null results. These same models found no change in these blood markers at the same-day or 1-day lag in the group without CVD. In 21 individuals with CVD, a 10 mug/m3 increase in same-day PM was associated with a 1.3 fold-rise [95% CI: 1.1, 1.7] in the level of monocyte chemoattractant protein-1. CONCLUSION: We did not find consistent effects of low ambient levels of PM on blood measures of inflammation or thrombosis in elderly individuals.

Abstract  There are no reported studies on the effects of ambient air pollution on emergency department (ED) attendances in Sydney, Australia. This study aimed to determine associations between ambient air pollutants and ED attendances for cardiovascular disease (CVD) in those aged 65+ years. We constructed daily time series of hospital ED attendances, air pollutants and meteorological factors for the Sydney metropolitan area from 1 January 1997 to 31 December 2001. We used generalised linear models to determine associations between daily air pollution and daily ED attendances and controlled for the effects of long-term trends, seasonality, weather and other potential confounders. Increased ED attendances for all CVD, cardiac disease and ischaemic heart disease were seen with 24-h particulate pollution, 1-h NO(2), 8-h CO and 24-h SO(2). Air pollutants were associated with decreased ED attendances for stroke. The effects of air pollutants on CVD, cardiac disease and stroke attendances were generally greater in the cool period compared to the warm period. The single-pollutant effects of CO, O(3), NO(2) and SO(2) were essentially unchanged in two-pollutant models. Although air pollution levels in Sydney are relatively low compared to similar cities, we have demonstrated associations between ambient air pollutants and ED attendances for CVD in people aged 65+ years. Our study adds to the growing evidence for the effects of ambient air pollution on CVD outcomes even at relatively low ambient concentrations.

Abstract  The case-crossover design was proposed for the study of a transient effect of an intermittent exposure on the subsequent occurrence of a rare acute-onset disease. This design can be an alternative to Poisson time series regression for studying the health effects of fine particulate matter air pollution. Characteristics of time-series of particulate matter, including long-term time trends, seasonal trends, and short-term autocorrelations, require that referent selection in the case-crossover design be considered carefully and adapted to minimize bias. We performed simulations to evaluate the bias associated with various referent selection strategies for a proposed case-crossover study of associations between particulate matter and primary cardiac arrest. Some a priori reasonable strategies were associated with a relative bias as large as 10%, but for most strategies the relative bias was less than 2% with confidence interval coverage within 1% of the nominal level. We show that referent selection for case-crossover designs raises the same issues as selection of smoothing method for time series analyses. In addition, conditional logistic regression analysis is not strictly valid for some case-crossover designs, introducing further bias.

Abstract  A variety of mitochondria have been observed to oxidize 13CO to 13CO2 in the presence of dioxygen, and on the basis of earlier studies [Young & Caughey (1986) Biochemistry 25, 152-161; Young (1981) Ph.D. Dissertation, Colorado State University] this activity is attributed to cytochrome c oxidase. Implications of these findings in respect of some aspects of the pathological biochemistry of CO poisoning are discussed.

Abstract  Eleven nonsmoking male resting subjects were exposed to two transient CO profiles to examine whether the resultant carboxyhemoglobin (HbCO) differs with CO concentration for a fixed total CO dose and to determine the predictive capability of the theoretical model of Coburn et al. (J. Clin. Invest. 44: 1899-1910, 1965) using measured alveolar ventilation. One profile consisted of five sequential exposures to 1,500 ppm CO for 5 min each and spaced 3 min apart. The other consisted of five sequential exposures to 7,500 ppm CO for 1 min each and spaced 7 min apart. The subjects, therefore, were exposed to the same overall nominal dose of 37,500 ppm.min. During the experiment, the subject's ventilatory functions and respiratory gases were recorded continuously, and the resultant HbCO% was measured in venous blood samples by gas chromatography. Mean increase (+/- SD) in HbCO% per exposure was 2.08 +/- 0.27% for the 1,500 ppm CO exposures and 2.05 +/- 0.29% for the 7,500 ppm CO exposures with no significant difference between the two. When the measured values of the subject's alveolar ventilation were applied to the theoretical model of Coburn et al., the predicted rate of HbCO% formation was found to agree with the experimental results.

Abstract  E.C. Environmental Research Programme, Bonn, Federal Republic of Germany.