Heat acclimatization and sunshine cause false indications of mortality due to ozone.

We used graphic analysis and generalized additive modeling to assess whether mortality that is often attributed to ozone and sometimes to < 10-microm particulate matter (PM10) and sulfur dioxide in hot weather results from confounding by neglected weather factors. When mean daily air temperatures exceeded 18 degrees C, mortality at age > or = 65 years, in Greater London 1991-2002 rose and at each temperature was generally higher in early summer than later after exposure to hot weather. Ozone, and to lesser degrees PM10 and sulfur dioxide, followed similar patterns. At each temperature, high levels of ozone and PM10 tended to be associated with sunshine, and high PM10 and sulfur dioxide with low wind, both of which will increase heat stress. With allowance for these confounding factors, generalized additive modeling showed no significant mortality due to ozone, to PM10, or to sulfur dioxide. We conclude that the pollutants played little part in excess mortality associated with hot weather.

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).

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.

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.

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.

Stricter ozone ambient air quality standard has beneficial effect on ponderosa pine in California.

Ambient air quality standards and control strategies are implemented to protect humans and vegetation from adverse effects. We used a process-based tree-growth model (TREGRO) to show that over the past 37 years, changes in O(3) exposure, with accompanying variation in climate, are reflected in changes in the growth of Pinus ponderosa Dougl. ex Laws. in the San Bernardino Mountains near Los Angeles, California, USA. Despite variation in temperature and precipitation over the study period (1963-1999), O(3) exposure consistently reduced simulated tree growth. Simulated growth reductions increased concurrent with increasing O(3) exposure. The maximum growth reduction occurred in 1979. As O(3) exposures decreased during the 1980s and 1990s, effects on growth also decreased. This implies that emission control strategies taken to reduce exposures to attain O(3) standards benefited P. ponderosa growth in the San Bernardino Mountains. This modeling approach provides a powerful tool for solving the difficult problem of evaluating regulatory effectiveness by simulating plant response using long-term climate and air pollution exposure records for a given region.

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.

Indoor exposures and acute respiratory effects in two general population samples from a rural and an urban area in Italy.

A study of indoor air exposures and acute respiratory effects in adults was conducted in the Po Delta (rural) and Pisa (urban) areas of Italy. Indoor exposures were monitored for nitrogen dioxide (NO(2)) and particulate matter <2.5 microm (PM(2.5)) for 1 week during the winter or summer in a total of 421 houses (2/3 in Pisa). Information on house characteristics, subjects' daily activity pattern and presence of acute respiratory symptoms was collected by a standardized questionnaire. Peak expiratory flow (PEF) maneuvers were performed by adult subjects four times daily; maximum amplitude and diurnal variation were taken into account. Indices of NO(2) and PM(2.5) exposures were computed as the product of weekly mean pollutant concentration by the time of daily exposure. Mean levels of pollutants were significantly higher in winter than in summer, regardless of the area. The relationship between exposure indices and acute respiratory symptoms was investigated only in winter. In spite of a slightly lower indoor level in the urban than in the rural area in winter (NO(2): 15 vs. 22 ppb; PM(2.5): 67 vs. 76 microg/m(3)), prevalence rates of acute respiratory symptoms were significantly higher in the urban than in the rural area. Acute respiratory illnesses with fever were significantly associated with indices of NO(2) (odds ratio (OR)=1.66; 95% CI=1.08-2.57) and PM(2.5) exposures (OR=1.62; 95% CI=1.04-2.51), while bronchitic/asthmatic symptoms were associated only with PM(2.5) (OR=1.39; 95% CI=1.17-1.66). PEF variability was positively related only to PM(2.5) exposure index (OR=1.38; 95% CI=1.24-1.54, for maximum amplitude; OR=1.37; 95% CI=1.23-1.53, for diurnal variation). In conclusion, indoor pollution exposures were associated with the presence of acute respiratory symptoms and mild lung function impairment in a rural and an urban area of Northern-Central Italy.

Determining the threshold effect of ozone on daily mortality: an analysis of ozone and mortality in Seoul, Korea, 1995-1999.

Many studies have shown a positive association between ambient ozone levels and mortality. Typically, these findings are based on models that assume a linear relationship between log mortality and ozone level. In this study, we adapted generalized additive models in which ozone effects are presumed to occur in three different ways: as a simple linear term, as a cubic natural spline term, and as a combination of two linear terms (a threshold model). We applied these models to daily time-series data for Seoul, Korea for the years 1995-1999 and found that the threshold model always fits best among the three. A 2.6% (95% CI: 1.7-3.5) increase of estimated relative risk (RR) in the total mortality associated with a 21.5 ppb increase of daily 1-h maximum ozone lagged by 1 day was observed by linear Poisson's regression. However, a 3.4% (95% CI: 2.3-4.4) increase in the estimated RR was observed using the threshold model. Adjustments for other ambient pollutants caused little changes to these results; 2.4-2.5% in the linear models and 3.2-3.4% in the threshold models. In addition, the largest difference in the estimated RRs of the linear and threshold models was observed in the summer: 1.9% (95% CI: 0.5-3.3) by the linear model and 3.8% (95% CI: 2.0-5.7) by the threshold model. These findings indicate that the conventional time-series Poisson regression model, which dose not take threshold into consideration, could underestimate the true risk of the ozone effect on daily mortality.

Association between ozone and respiratory admissions among children and the elderly in Vancouver, Canada.

In this study, we examine the impact of ozone on daily respiratory admissions in both young children and the elderly in greater Vancouver, British Columbia. Study subjects included children less than 3 yr of age and adults 65 yr of age or over living in greater Vancouver who had acute hospital admissions for any respiratory diseases (ICD-9 codes 460-519) during the 13-yr period 1986-1998. Bidirectional case-crossover analysis was used to investigate associations between ambient ozone and respiratory hospitalizations after adjustment for other pollutants, including carbon monoxide, nitrogen dioxide, sulfur dioxide, and coefficient of haze. Potential effect modification by socioeconomic status as measured by household income was also examined. Respiratory admissions were associated with ozone levels 2, 3, 4, and 5 days prior to admission in both children and the elderly, with the strongest association observed at a lag of 4 days. Odds ratios for hospital admission of 1.22 (95% CI: 1.15-1.30) for children and 1.13 (1.09-1.18) for the elderly, respectively, were found, based on an increment in exposure corresponding to the interquartile range for ozone. Adjusting for other pollutants did not attenuate the ozone effect on respiratory admissions. Nor did socioeconomic status appear to modify the association between ozone and respiratory admissions in either children or the elderly. We concluded that ambient ozone is positively associated with respiratory hospital admission among young children and the elderly in Vancouver, British Columbia. These associations persisted after adjustment for both copollutant exposures and socioeconomic status.

Development of an assay for ozone-specific antioxidant capacity.

A method of determining the ozone-specific antioxidant capacity (OZAC) of lavage samples from the respiratory system was developed: Gaseous ozone (O(3)) was produced in cuvettes by irradiation with an ultraviolet lamp; aliquots of sample or of a saline control were then added and sufficient time was allowed for ozonation to reach completion; and an aliquot of indigo trisulfonate (ITS) was added to react with excess O(3). Because each molecule of O(3) rapidly bleaches one molecule of the deeply colored ITS, an OZAC value in concentration units was computed from the difference in light absorbance between the sample and the saline control multiplied by the extinction coefficient of ITS. Experiments in 0-40 micro M antioxidant solutions indicated that the OZAC values of uric acid and ascorbic acid were close to their actual concentrations and were independent of O(3) concentration. On the other hand, the OZAC of reduced glutathione and possibly human nasal lavage were nonlinearly related to antioxidant concentration and were directly related to O(3) concentration.

The Po River Delta (north Italy) indoor epidemiological study: effects of pollutant exposure on acute respiratory symptoms and respiratory function in adults.

The authors studied the effects of relatively low doses of nitrogen dioxide and respirable suspended particulate matter (i.e., < 2.5 mu) on acute respiratory symptoms and on peak expiratory flow in 383 adults (15-72 yr of age) who lived in the Po River Delta area, located near Venice. During 2 wk-1 wk in winter and 1 wk in summer--the authors monitored each participant's house to measure nitrogen dioxide (in parts per billion) and respirable suspended particulate (microgram/m3) concentration. Information on sex, age, height, weight, daily activity patterns, active and passive smoking, chronic respiratory diseases, daily peak expiratory flow, and presence of acute respiratory symptoms during the weeks monitoring occurred were also collected. Peak expiratory flow variation was studied as mean amplitude percentage (i.e., amplitude/mean) and percentage of diurnal variation (maximum/minimum). The exposure indices to nitrogen dioxide (nitrogen dioxide--index of exposure) and to respirable suspended particulate matter (respirable suspended particulate matter-index of exposure) were computed as the product of pollutant concentration and time of exposure. The authors considered indices as "low" or "high" on the basis of the median value. The median nitrogen dioxide was 20 ppb in winter and 14 ppb in summer; the highest nitrogen dioxide levels occurred in the kitchen in the winter (33 ppb) and summer (20 ppb). The median respirable suspended particulate matter was 68 micrograms/m3 in winter and 45 micrograms/m3 in summer. Only in winter were there significant associations between bronchitic/asthmatic symptoms and "high" nitrogen dioxide and respirable suspended particulate matter indices. In subjects who did not smoke, a significant influence of the "high" respirable suspended particulate matter-index of exposure was also observed in summer. With respect to peak expiratory flow and its variability, respirable suspended particulate matter-index of exposure was associated with an increase of both amplitude/mean and maximum/mean; however, with respect to the nitrogen dioxide--index of exposure, the association was significant only in subjects with chronic respiratory diseases (i.e., asthma and bronchitis). These relationships were significant only in winter. In conclusion, the results of the current study indicate that there is an association between relatively low doses of pollutants and acute respiratory symptoms and peak expiratory flow in adults.

Genetic modeling of susceptibility to nitrogen dioxide-induced lung injury in mice.

We investigated the mode of inheritance of susceptibility to nitrogen dioxide (NO2)-induced lung injury in inbred mice. Susceptible C57BL/6J (B6) and resistant C3H/HeJ (C3) mice, as well as F1, F2, and backcross (BX) populations derived from them, were exposed to 15 parts per million NO2 for 3 h. Six hours after exposure, animals were lavaged, and differential cell counts and cell viability (cytotoxicity) were measured. Statistically significant (P < 0.05) differences in numbers of lavageable macrophages, epithelial cells, and dead cells were found between inbred strains. Distributions of cellular responses in F1 progeny overlapped both progenitors, and mean responses were intermediate. In C3:BX progeny, ranges of responses to NO2 closely resembled C3 mice, and means were not significantly different between populations. Ranges of cellular responses to NO2 in B6:BX and intercross progeny overlapped both progenitors; mean responses of both populations were intermediate to progenitors. Segregation analyses tested goodness of fit of phenotyping data with various inheritance models, and the highest likelihood for each cell response to NO2 was for the hypothesis two-unlinked loci general. We conclude that there are likely two major unlinked genes that account for differential susceptibility to acute NO2 exposure. The chromosomal location of the genes is not known.

Growth response of bigcone Douglas fir (Pseudotsuga macrocarpa) to long-term ozone exposure in southern California.

Long-term radial growth of bigcone Douglas fir (Pseudotsuga macrocarpa) was studied throughout its range in the San Bernardino Mountains of southern California, where ambient ozone has been high for approximately the past 40 years. A gradient of both ozone concentration and precipitation exists from west (high) to east (low). Growth rates of bigcone Douglas fir are considerably lower since 1950 throughout the San Bernardino Mountains, with the largest growth reductions in the western part of the range where ozone exposure is highest. Needle retention is also somewhat lower at high ozone sites. Lower annual precipitation since 1950 may have some impact on long-term growth reductions, and short-term growth reductions induced by drought are an important component of long-term growth reductions at sites with high ozone exposure. An ozone-climate stress complex may be responsible for recent reductions in the growth of bigcone Douglas fir.

The risk of photochemical reactions.

In January 1987, an incident occurred at a petrochemical complex in Salavat, Russia. The incident resulted in the poisoning of 17 people by the products of photochemical smog. This paper describes the incident and discusses the possibility of chemical reactions that pose toxic hazardous situations for chemical plant personnel. Pollutants present in the atmosphere as a result of continuous releases can result in the formation of toxic substances and the poisoning of people, even when permissible levels of concentrations are not exceeded for the initial pollutants. In addition, this paper addresses the need to consider the possibility of secondary chemical reactions in the environment while planning chemical plant activity.

Athletic performance and urban air pollution.

Air pollution may affect athletic performance. In Los Angeles, contaminants include carbon monoxide, ozone, peroxyacetylnitrate (PAN) and nitrogen oxides, whereas in older European cities, such as Sarajevo, "reducing smog" of sulfur dioxide is the main hazard. The carbon monoxide and ozone levels expected in Los Angeles this summer could affect the athletes' performance in endurance events at the Olympic Games. Carbon monoxide may also impair psychomotor abilities, and PAN causes visual disturbances. The only likely physiologic consequence from reducing smog is an increase in the workload of the respiratory system and thus a decrease in endurance performance. While carbon monoxide has been blamed for myocardial infarctions, nitrogen oxides for pulmonary edema and sulfur dioxide for deaths due to respiratory failure, the only illnesses that are likely to be more frequent than usual among young athletes exposed to high levels of these pollutants are upper respiratory tract infections. Therapeutic tactics include the avoidance of pollution, the administration of oxygen, vitamin C and vitamin E, and general reassurance.