Impacts and mitigation of excess diesel-related NOx emissions in 11 major vehicle markets.

Vehicle emissions contribute to fine particulate matter (PM2.5) and tropospheric ozone air pollution, affecting human health, crop yields and climate worldwide. On-road diesel vehicles produce approximately 20 per cent of global anthropogenic emissions of nitrogen oxides (NOx), which are key PM2.5 and ozone precursors. Regulated NOx emission limits in leading markets have been progressively tightened, but current diesel vehicles emit far more NOx under real-world operating conditions than during laboratory certification testing. Here we show that across 11 markets, representing approximately 80 per cent of global diesel vehicle sales, nearly one-third of on-road heavy-duty diesel vehicle emissions and over half of on-road light-duty diesel vehicle emissions are in excess of certification limits. These excess emissions (totalling 4.6 million tons) are associated with about 38,000 PM2.5- and ozone-related premature deaths globally in 2015, including about 10 per cent of all ozone-related premature deaths in the 28 European Union member states. Heavy-duty vehicles are the dominant contributor to excess diesel NOx emissions and associated health impacts in almost all regions. Adopting and enforcing next-generation standards (more stringent than Euro 6/VI) could nearly eliminate real-world diesel-related NOx emissions in these markets, avoiding approximately 174,000 global PM2.5- and ozone-related premature deaths in 2040. Most of these benefits can be achieved by implementing Euro VI standards where they have not yet been adopted for heavy-duty vehicles.

The contribution of outdoor air pollution sources to premature mortality on a global scale.

Assessment of the global burden of disease is based on epidemiological cohort studies that connect premature mortality to a wide range of causes, including the long-term health impacts of ozone and fine particulate matter with a diameter smaller than 2.5 micrometres (PM2.5). It has proved difficult to quantify premature mortality related to air pollution, notably in regions where air quality is not monitored, and also because the toxicity of particles from various sources may vary. Here we use a global atmospheric chemistry model to investigate the link between premature mortality and seven emission source categories in urban and rural environments. In accord with the global burden of disease for 2010 (ref. 5), we calculate that outdoor air pollution, mostly by PM2.5, leads to 3.3 (95 per cent confidence interval 1.61-4.81) million premature deaths per year worldwide, predominantly in Asia. We primarily assume that all particles are equally toxic, but also include a sensitivity study that accounts for differential toxicity. We find that emissions from residential energy use such as heating and cooking, prevalent in India and China, have the largest impact on premature mortality globally, being even more dominant if carbonaceous particles are assumed to be most toxic. Whereas in much of the USA and in a few other countries emissions from traffic and power generation are important, in eastern USA, Europe, Russia and East Asia agricultural emissions make the largest relative contribution to PM2.5, with the estimate of overall health impact depending on assumptions regarding particle toxicity. Model projections based on a business-as-usual emission scenario indicate that the contribution of outdoor air pollution to premature mortality could double by 2050.

Short-term association between exposure to ozone and mortality in Oporto, Portugal.

Exposures to air pollution in developed countries have generally decreased over the last two decades. However, many recent epidemiological studies have consistently shown positive associations between low-level exposure to air pollutants and health outcomes. In Portugal, very few studies have analysed the acute effect of air pollutants on health. The present study evaluates the association between exposure to air pollution and daily mortality in the Oporto Metropolitan Area, Portugal. Generalised additive models were used for this analysis. Pollutants assessed were ozone, nitrogen dioxide, and particulate matter (PM(10)). Models were adjusted for time trend, seasonality, and weather. We report that an increase of 10 µg/m(3) in the daily ozone 8-h maximum moving-average corresponds to an increase of 0.95% (95%CI: 0.30, 1.60) and 1.58% (95%CI: 0.45, 2.73) in non-accidental mortality and cardiovascular mortality, respectively, in the summer season. A significant effect of 0.67% (95% CI: 0.03:1.32) was also found for the association between PM(10) and non-accidental mortality in the summer season. Associations with ozone and PM(10) exposures were higher in the elderly people. No significant effects on mortality were observed during the summer season with nitrogen dioxide exposures. Our analyses provide the first significant evidence in Oporto that exposures to O(3) and PM(10) have adverse effects on the health of the general population in the summer months.

Acute effects of air pollution on pediatric asthma exacerbation: evidence of association and effect modification.

We investigated the short-term effects of particulate matter with aerodynamic diameter <10 µg/m(3) (PM(10)), sulfur dioxide (SO(2)), nitrogen dioxide (NO(2)) and ozone (O(3)) on pediatric asthma emergency admissions in Athens, Greece over the period 2001-2004. We explored effect modification patterns by season, sex, age and by the presence of desert dust transported mainly from the Sahara area. We used daily time-series data provided by the children's hospitals and the fixed monitoring stations. The associations were investigated using Poisson regression models controlling for seasonality, weather, influenza episodes, day of the week and holiday effects. A 10 µg/m(3) increase in PM(10) was associated with a 2.54% increase (95% confidence interval (CI): 0.06%, 5.08%) in the number of pediatric asthma hospital admissions, while the same increase in SO(2) was associated with a 5.98% (95% CI: 0.88%, 11.33%) increase. O(3) was associated with a statistically significant increase in asthma admissions among older children in the summer. Our findings provide limited evidence of an association between NO(2) exposure and asthma exacerbation. Statistically significant PM(10) effects were higher during winter and during desert dust days, while SO(2) effects occurred mainly during spring. Our study confirms previously reported PM(10) effects on emergency hospital admissions for pediatric asthma and further provides evidence of stronger effects during desert dust days. We additionally report severe effects of SO(2), even at today's low concentration levels.

Ambient air pollution and congenital heart disease: a register-based study.

Maternal exposure to ambient air pollution has increasingly been linked to adverse pregnancy outcomes. The evidence linking this exposure to congenital anomalies is still limited and controversial. This case-control study investigated the association between maternal exposure to ambient particulate matter with aerodynamic diameter less than 10 µm (PM(10)), sulfur dioxide (SO(2)), nitrogen dioxide, nitric oxide (NO), ozone (O(3)), and carbon monoxide (CO) and the occurrence of congenital heart disease in the population of Northeast England (1993-2003). Each case and control was assigned weekly average (weeks 3-8 of pregnancy) of pollutant levels measured by the closest monitor to the mother's residential postcode. Using exposure as both continuous and categorical variables, logistic regression models were constructed to quantify the adjusted odds ratios of exposure to air pollutants and the occurrence of each outcome group. We found exposure to CO and NO to be associated with ventricular septal defect and cardiac septa malformations. CO was also associated with congenital pulmonary valve stenosis and NO with pooled cases of congenital heart disease and tetralogy of Fallot. Findings for SO(2), O(3) and PM(10) were less consistent.

Residential mobility during pregnancy and the potential for ambient air pollution exposure misclassification.

Studies of environmental exposures and adverse birth outcomes often rely on maternal address at birth obtained from the birth certificate to classify exposure. Although the gestational age of interest is often early pregnancy, maternal addresses are not available for women who move during pregnancy when using maternal addresses abstracted from birth certificates. The aim of this study was to explore the extent of ambient air pollutant exposure misclassification due to maternal residential mobility during pregnancy among the subgroup of a New York birth cohort. The authors obtained the maternal addresses at birth from the New York Birth Certificate, and the maternal addresses by gestational age from the National Birth Defect Prevention Study for New York participants for the study period 1997-2002. Among the 1324 mothers, 172 (13.0%) moved once during pregnancy and 46 (3.5%) moved at least twice. When accounting for multiple addresses among some individuals, of the 218 mothers who moved, 38 (2.9%) moved in the 3rd to 8th weeks after conception (critical period, not exclusive from the 1st trimester), 80 (6.0%) moved in the 1st trimester, 112 (8.5%) in the 2nd trimester, and 51 (3.9%) in the 3rd trimester. Air monitoring data from the New York Department of Environmental Conservation were used as surrogates to compute the ambient ozone and PM(10) exposures for mothers with complete residential data. This study estimates exposure using maternal address at birth obtained from birth certificates, compared to exposure estimates when using maternal addresses by gestational age obtained from maternal interview, the gold standard. Average exposures during pregnancy were similar when using interview based versus birth certificate addresses (0.035 vs. 0.035 ppm for ozone, and 20.11 vs. 20.09 microg/m(3) for PM(10), respectively). Kappa statistics and percent agreement were calculated to measure the degree of agreement for dichotomous exposure measurements (=median) and weighted kappa for quartile exposure measurements by gestational age. All the statistics indicated a high agreement between the two measurements. For mothers who moved, the majority maintained their address in the same exposure region. Given the low mobility during pregnancy and the short distance moved, the exposure assignment did not change substantially when using the more accurate interview based addresses in this study. However, the level of observed agreement may decrease for studies that require smaller geographic zones for exposure assignments or with more mobile study populations.

Temperature-dependent association between mortality rate and carbon monoxide level in a subtropical city: Kaohsiung, Taiwan.

The objective of this study was to explore the combined effect of temperature and air pollutant levels on daily non-accidental deaths and cardiovascular causes of mortality. In this study, associations were assessed by means of time-series analyses over the period 1995-1999 for Kaohsiung, Taiwan's largest industrial city, which has a subtropical climate. Ambient exposures to various air pollutants, including carbon monoxide (CO), sulfur dioxide (SO(2)), ozone (O(3)), nitrogen dioxide (NO(2)), and particulate matter (PM(10)), were estimated from the arithmetic means of all daily measurements taken by an air quality monitoring station nearest to the residential district. Generalized additive models with non-parametric spline were used to identify associations between daily mortality and air pollutants as well as the air pollutant-temperature interaction correlation. Our findings indicate that CO is associated with increased risks of non-accidental and cardiovascular mortality. For a 0.2 ppm increase in CO, the increased relative daily risk of non-accidental death is at least 4% on the same day, when the mean temperature is above 24.8 degrees C, while the increased relative risk of mortality due to cardiovascular diseases is 7% two days later at 19.7 degrees C. The study also suggests a statistically significant interaction between CO concentration and daily mean temperature, with non-accidental mortality increasing with a warm outdoor temperature and the effect of CO on cardiovascular mortality being modified by a cold climate. Further reduction of CO pollution is thus deemed crucial for the benefit of public health.

Fluticasone propionate protects against ozone-induced airway inflammation and modified immune cell activation markers in healthy volunteers.

BACKGROUND: Ozone exposure induces airway neutrophilia and modifies innate immune monocytic cell-surface phenotypes in healthy individuals. High-dose inhaled corticosteroids can reduce O(3)-induced airway inflammation, but their effect on innate immune activation is unknown. OBJECTIVES: We used a human O(3) inhalation challenge model to examine the effectiveness of clinically relevant doses of inhaled corticosteroids on airway inflammation and markers of innate immune activation in healthy volunteers. METHODS: Seventeen O(3)-responsive subjects [>10% increase in the percentage of polymorphonuclear leukocytes (PMNs) in sputum, PMNs per milligram vs. baseline sputum] received placebo, or either a single therapeutic dose (0.5 mg) or a high dose (2 mg) of inhaled fluticasone proprionate (FP) 1 hr before a 3-hr O(3) challenge (0.25 ppm) on three separate occasions at least 2 weeks apart. Lung function, exhaled nitric oxide, sputum, and systemic biomarkers were assessed 1-5 hr after the O(3) challenge. To determine the effect of FP on cellular function, we assessed sputum cells from seven subjects by flow cytometry for cell-surface marker activation. RESULTS: FP had no effect on O(3)-induced lung function decline. Compared with placebo, 0.5 mg and 2 mg FP reduced O(3)-induced sputum neutrophilia by 18% and 35%, respectively. A similar effect was observed on the airway-specific serum biomarker Clara cell protein 16 (CCP16). Furthermore, FP pretreatment significantly reduced O(3)-induced modification of CD11b, mCD14, CD64, CD16, HLA-DR, and CD86 on sputum monocytes in a dose-dependent manner. CONCLUSIONS: This study confirmed and extended data demonstrating the protective effect of FP against O(3)-induced airway inflammation and immune cell activation.

Impact of high temperatures on hospital admissions: comparative analysis with previous studies about mortality (Madrid).

BACKGROUND: Heat wave prevention plans are traditionally implemented according to a temperature limit above which mortality begins to rise. Although these prevention plans are obviously designed to avoid deaths, it is also necessary to establish the impact of extreme temperatures on hospital admissions in order to put hospital alert plans into action for dealing with people affected by heat wave victims. METHODS: We used data on daily emergency admissions between May and September, from 1995 to 2000, in the Hospital General Universitario Gregorio Marañón in Madrid. The causes for admission were considered as 'organic' (International Classification of Diseases, ICD-9: 1-799), circulatory (ICD-9: 390-459) and respiratory (ICD-9: 460-519). We stratified them according to the following age groups: all ages, from 0 to 10, 18 to 44, 45 to 64, 65 to 74 and above 75 years. The methodology used was Autorregresive Integrated Moving Average (ARIMA) modelling, including variables related to atmospheric pollution, seasonality and trends. RESULTS: The results show that the temperature above which hospital admissions soar coincides with the temperature limit above which mortality sharply rises, which, in turn, coincides with percentile 95 of the maximum daily temperature series for summer months. The pattern of hospital admissions is completely different from that of mortality. The rise in hospital admissions due to all causes and age groups is clearly smaller than that detected for mortality. DISCUSSION: These results suggest that people die rapidly from circulatory diseases before they can be admitted to hospital. This datum is vital with regard to implementing prevention plans prior to the arrival of the heat wave, if they are to effectively reduce mortality.

Effects of chronic and acute ozone exposure on lipid peroxidation and antioxidant capacity in healthy young adults.

BACKGROUND: There is growing evidence for the role of oxidative damage in chronic diseases. Although ozone (O3) is an oxidant pollutant to which many people are exposed, few studies have examined whether O3 induces oxidative stress in humans. OBJECTIVES: This study was designed to assess the effect of short-and long-term O(3) exposures on biomarkers of oxidative stress in healthy individuals. METHODS: Biomarkers of lipid peroxidation, 8-isoprostane (8-iso-PGF), and antioxidant capacity ferric reducing ability of plasma (FRAP) were analyzed in two groups of healthy college students with broad ranges of ambient O3 exposure during their lifetimes and previous summer recess either in Los Angeles (LA, n = 59) or the San Francisco Bay Area (SF, n = 61). RESULTS: Estimated 2-week, 1-month, and lifetime O3 exposures were significantly correlated with elevated 8-iso-PGF. Elevated summertime exposures resulted in the LA group having higher levels of 8-iso-PGF than the SF group (p = 0.02). Within each location, males and females had similar 8-iso-PGF. No regional difference in FRAP was observed, with significantly higher FRAP in males in both groups (SF: p = 0.002; LA: p = 0.004). An exposure chamber substudy (n = 15) also showed a significant increase in 8-iso-PGF as well as an inhibition of FRAP immediately after a 4-hr exposure to 200 ppb O3, with near normalization by 18 hr in both biomarkers. CONCLUSIONS: Long-term exposure to O3 is associated with elevated 8-iso-PGF, which suggests that 8-iso-PGF is a good biomarker of oxidative damage related to air pollution.

Effects of air pollution on heart rate variability: the VA normative aging study.

Reduced heart rate variability (HRV), a marker of poor cardiac autonomic function, has been associated with air pollution, especially fine particulate matter [< 2.5 microm in aerodynamic diameter (PM2.5)]. We examined the relationship between HRV [standard deviation of normal-to-normal intervals (SDNN), power in high frequency (HF) and low frequency (LF), and LF:HF ratio] and ambient air pollutants in 497 men from the Normative Aging Study in greater Boston, Massachusetts, seen between November 2000 and October 2003. We examined 4-hr, 24-hr, and 48-hr moving averages of air pollution (PM2.5, particle number concentration, black carbon, ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide). Controlling for potential confounders, HF decreased 20.8% [95% confidence interval (CI), 4.6-34.2%] and LF:HF ratio increased 18.6% (95% CI, 4.1-35.2%) per SD (8 microg/m3) increase in 48-hr PM2.5. LF was reduced by 11.5% (95% CI, 0.4-21.3%) per SD (13 ppb) increment in 4-hr O3. The associations between HRV and PM2.5 and O3 were stronger in people with ischemic heart disease (IHD) and hypertension. The associations observed between SDNN and LF and PM2.5 were stronger in people with diabetes. People using calcium-channel blockers and beta-blockers had lower associations between O3 and PM2.5 with LF. No effect modification by other cardiac medications was found. Exposures to PM2.5 and O3 are associated with decreased HRV, and history of IHD, hypertension, and diabetes may confer susceptibility to autonomic dysfunction by air pollution.

Sputum induction and bronchoscopy for assessment of ozone-induced airway inflammation in asthma.

BACKGROUND: Neutrophilic airway inflammation, as defined by cell counts in respiratory tract lining fluid (RTLF), is a key end point in many studies of respiratory toxicity in both healthy and asthmatic subjects. BAL and sputum induction (SI) are the most common methods of sampling RTLF in such studies. However, the comparability of these methods (BAL and SI) after experimental treatment has not been investigated in a head-to-head controlled trial. METHODS: To determine whether BAL and SI are comparable and can be used in place of each other in the assessment of neutrophilic airway inflammation after ozone (O(3)) exposure, we exposed 13 asthmatic subjects to either 0.2 ppm of O(3) or filtered air (FA) followed by either BAL or SI. Subjects then underwent the alternate (O(3) or FA) exposure followed by the same method of RTLF sampling. Next, subjects repeated the same exposure protocol with the alternate method of RTLF sampling. Differences in inflammatory indexes including the percentage of polymorphonuclear neutrophils (%PMNs) between the exposures were then correlated by regression analysis. RESULTS: The %PMNs in sputum was poorly correlated with that in BAL fluid (R = 0.12). The correlation between the %PMNs in sputum and in the bronchial fraction of BAL (BFx) fluid, however, was somewhat higher (R = 0.50). Furthermore, the uncertainty of the estimate of %PMN values in BFx fluid and BAL fluid based on those of sputum values, using regression models, was almost as great as the magnitude of the O(3) effect itself (ie, 9.7% and 5.5% estimate errors for O(3) effects of 17.0% and 7.5%, respectively). CONCLUSION: We concluded that SI and BAL indexes are not directly interchangeable in the assessment of O(3)-induced airway inflammation in asthmatic subjects.

The effects of outdoor air pollution and tobacco smoke on asthma.

Outdoor air pollution and environmental tobacco smoke adversely affect health in persons with asthma. Increased levels of ozone, particulate matter, and environmental tobacco smoke have been associated with increased asthma symptoms and health care use and with reduced lung function. These air contaminants have proinflammatory actions that can magnify existing lower airway inflammation in patients with asthma. Exposure to air contaminants can increase the risk of developing asthma in susceptible persons. Outdoor air pollution and environmental tobacco smoke may affect allergen-induced inflammation by initiating TH(2) responses to antigens or by exacerbating such inflammation in persons already sensitized.

The effects of air pollution and meteorological parameters on respiratory morbidity during the summer in São Paulo City.

Effects of meteorological variables and air pollutants on child respiratory morbidity are investigated during two consecutive summers (December-March 1992/1993 and 1993/1994) at the Metropolitan Area of São Paulo (MASP), Brazil. The MASP, with almost 17 million inhabitants, is considered the most populous region in South America. Due to warmer temperatures, increased rainfall and consequent low levels of air pollutants during the summer compared to winter, less attention has been paid to epidemiological studies during this season, especially in tropical urban areas such as São Paulo. In the present work, principal component analysis (PCA) is applied to medical end environmental data to identify patterns relating child morbidity, meteorological variables and air pollutants during the summer. The following pollutant concentrations are examined: SO2, inhalable particulate matter (PM10), and O3. The meteorological variables investigated are air temperature, water vapor (water vapor density) and solar radiation. Although low correlation between respiratory morbidity and environmental variables are, in general, observed for the entire dataset, the PCA method indicates that child morbidity is positively associated with O3 for the 1992/1993 summer. This pattern is identified in the third principal component (PC3), which explains about 19% of the total variance of all data in this summer. However, the 1993/1994 summer shows a more complex association between both groups, suggesting stronger ties with meteorological variables. Marked changes in synoptic conditions from the end of January to end of March of the 1993/1994 summer seem to have played an important role in modulating respiratory morbidity. A detailed examination of meteorological conditions in that period indicates that prefrontal (postfrontal), hot (cold) and dry (wet) days favored the observed decrease (increase) of respiratory morbidity.

Metrics matter: conflicting air quality rankings from different indices of air pollution.

Comparisons of air quality policies involve numerous considerations such as cost, health, effects on vegetation and materials, and aesthetics. Such assessments require difficult scientific and value judgments. These difficulties can also characterize comparisons that consider only physical and chemical air quality indices. We compare ambient tropospheric ozone concentrations from a baseline scenario and seven emissions scenarios for a case study. The resulting air qualities are evaluated based upon spatial and temporal distribution of impacts, exceedances of regulatory standards, concentrations weighted by population density, and a variety of averaging times. Results reveal that even when only a single pollutant is considered, comparisons of air quality can be ambiguous. Which scenario has better air quality depends on how (e.g., choice of averaging times, absolute vs. relative changes in concentrations), where (e.g., effects in specific areas vs. effects over the entire region), and when (e.g., the percent of time for which one alternative has higher concentrations than another) the comparison is made. This indicates that general descriptors of air quality such as the annual average ozone concentration do not fully describe the complexity of air quality. Use of such averages can result in different policy rankings than consideration of the full distribution of impacts.

Economic assessment of the negative impacts of ozone on crop yields and forest production. A case study of the estate Ostads Säteri in southwestern Sweden.

Ground level ozone concentrations, in combination with the prevailing climate, at the estate Ostads Säteri in southwestern Sweden were estimated to reduce the yield of wheat and potato ranging between 5% and 10%. Occasionally, in years with the highest ozone concentrations and/or climatic conditions favoring high rates of ozone uptake to the leaves, yield loss levels above 10% may occur. Based on simple extrapolation, these ozone-induced reductions of crop yields at Ostads Säteri represent a potential total annual yield loss in Sweden in the range of 24.5 million Euro for wheat and 7.3 million Euro for potato, respectively. A simulation of forest growth at Ostad Säteri predicted that prevailing mean ozone exposure during 1993-2003 had the potential to reduce forest growth by 2.2% and the economic return of forest production by 2.6%. Using this value for extrapolation to the national level, the potential annual economic loss for Sweden due to negative impacts of ozone on forest production would be in the range of 56 million Euro (2004 prices).

Association of FEV1 in asthmatic children with personal and microenvironmental exposure to airborne particulate matter.

Exposure to particulate matter (PM) air pollution has been shown to exacerbate children's asthma, but the exposure sources and temporal characteristics are still under study. Children's exposure to PM is likely to involve both combustion-related ambient PM and PM related to a child's activity in various indoor and outdoor microenvironments. Among 19 children with asthma, 9-17 years of age, we examined the relationship of temporal changes in percent predicted forced expiratory volume in 1 sec (FEV1) to personal continuous PM exposure and to 24-hr average gravimetric PM mass measured at home and central sites. Subjects were followed for 2 weeks during either the fall of 1999 or the spring of 2000, in a southern California region affected by transported air pollution. FEV(subscript)1(/subscript) was measured by subjects in the morning, afternoon, and evening. Exposure measurements included continuous PM using a passive nephelometer carried by subjects; indoor, outdoor home, and central-site 24-hr gravimetric PM2.5 (PM of aerodynamic diameter < 2.5 microm) and PM10; and central-site hourly PM10, nitrogen dioxide, and ozone. Data were analyzed with linear mixed models controlling for within-subject autocorrelation, FEV1 maneuver time, and exposure period. We found inverse associations of FEV1 with increasing PM exposure during the 24 hr before the FEV1 maneuver and with increasing multiday PM averages. Deficits in percent predicted FEV1 (95% confidence interval) for given PM interquartile ranges measured during the preceding 24-hr were as follows: 128 microg/m3 1-hr maximum personal PM, -6.0% (-10.5 to -1.4); 30 microg/m3 24-hr average personal PM, -5.9% (-10.8 to -1.0); 6.7 microg/m3 indoor home PM2.5, -1.6% (-2.8 to -0.4); 16 microg/m3 indoor home PM10, -2.1% (-3.7 to -0.4); 7.1 microg/m3 outdoor home PM2.5, -1.1% (-2.4 to 0.1); and 7.5 microg/m3 central-site PM2.5, -0.7% (-1.9 to 0.4). Stronger associations were found for multiday moving averages of PM for both personal and stationary-site PM. Stronger associations with personal PM were found in boys allergic to indoor allergens. FEV1 was weakly associated with NO2 but not with O3. Results suggest mixed respiratory effects of PM in asthmatic children from both ambient background exposures and personal exposures in various microenvironments.

Pulmonary epithelial integrity in children: relationship to ambient ozone exposure and swimming pool attendance.

Airway irritants such as ozone are known to impair lung function and induce airway inflammation. Clara cell protein (CC16) is a small anti-inflammatory protein secreted by the nonciliated bronchiolar Clara cells. CC16 in serum has been proposed as a noninvasive and sensitive marker of lung epithelial injury. In this study, we used lung function and serum CC16 concentration to examine the pulmonary responses to ambient O3 exposure and swimming pool attendance. The measurements were made on 57 children 10-11 years of age before and after outdoor exercise for 2 hr. Individual O3 exposure was estimated as the total exposure dose between 0700 hr until the second blood sample was obtained (mean O3 concentration/m3 times symbol hours). The maximal 1-hr value was 118 microg/m3 (59 ppb), and the individual exposure dose ranged between 352 and 914 microg/m3hr. These O3 levels did not cause any significant changes in mean serum CC16 concentrations before or after outdoor exercise, nor was any decrease in lung function detected. However, children who regularly visited chlorinated indoor swimming pools had significantly lower CC16 levels in serum than did nonswimming children both before and after exercise (respectively, 57 +/- 2.4 and 53 +/- 1.7 microg/L vs. 8.2 +/- 2.8 and 8.0 +/- 2.6 microg/L; p < 0.002). These results indicate that repeated exposure to chlorination by-products in the air of indoor swimming pools has adverse effects on the Clara cell function in children. A possible relation between such damage to Clara cells and pulmonary morbidity (e.g., asthma) should be further investigated.

Assessing ozone-related health impacts under a changing climate.

Climate change may increase the frequency and intensity of ozone episodes in future summers in the United States. However, only recently have models become available that can assess the impact of climate change on O3 concentrations and health effects at regional and local scales that are relevant to adaptive planning. We developed and applied an integrated modeling framework to assess potential O3-related health impacts in future decades under a changing climate. The National Aeronautics and Space Administration-Goddard Institute for Space Studies global climate model at 4 degrees x 5 degrees resolution was linked to the Penn State/National Center for Atmospheric Research Mesoscale Model 5 and the Community Multiscale Air Quality atmospheric chemistry model at 36 km horizontal grid resolution to simulate hourly regional meteorology and O3 in five summers of the 2050s decade across the 31-county New York metropolitan region. We assessed changes in O3-related impacts on summer mortality resulting from climate change alone and with climate change superimposed on changes in O3 precursor emissions and population growth. Considering climate change alone, there was a median 4.5% increase in O3-related acute mortality across the 31 counties. Incorporating O3 precursor emission increases along with climate change yielded similar results. When population growth was factored into the projections, absolute impacts increased substantially. Counties with the highest percent increases in projected O3 mortality spread beyond the urban core into less densely populated suburban counties. This modeling framework provides a potentially useful new tool for assessing the health risks of climate change.

Air pollution and daily mortality in a city with low levels of pollution.

The concentration-response relationship between daily ambient inhalable particle (particulate matter less than or equal to 10 micro m; PM(10)) concentrations and daily mortality typically shows no evidence of a threshold concentration below which no relationship is observed. However, the power to assess a relationship at very low concentrations of PM(10) has been limited in studies to date. The concentrations of PM(10) and other air pollutants in Vancouver, British Columbia, Canada, from January 1994 through December 1996 were very low: the 50th and 90th percentiles of daily average PM(10) concentrations were 13 and 23 micro g/m(3), respectively, and 27 and 39 ppb, respectively, for 1-hr maximum ozone. Analyses of 3 years of daily pollution (PM(10), ozone, sulfur dioxide, nitrogen dioxide, and carbon monoxide) concentrations and mortality counts showed that the dominant associations were between ozone and total mortality and respiratory and cardiovascular mortality in the summer, and between nitrogen dioxide and total mortality in the winter, although some association with PM(10) may also have been present. We conclude that increases in low concentrations of air pollution are associated with increased daily mortality. These findings may support the notion that no threshold pollutant concentrations are present, but they also raise concern that these effects may not be effects of the measured pollutants themselves, but rather of some other factor(s) present in the air pollution-meteorology mix.