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Environmental Health Perspectives Volume 109, Supplement 3, June 2001

Assessing the Health Benefits of Urban Air Pollution Reductions Associated with Climate Change Mitigation (2000-2020): Santiago, São Paulo, México City, and New York City 

Luis Cifuentes,1 Victor H. Borja-Aburto,2 Nelson Gouveia,3 George Thurston,4 and Devra Lee Davis

1Pontificia Universidad Católica de Chile, Santiago, Chile; 2Secretaria de Salud, Ciudad de México, México; 3Departamento de Medicina Preventiva, Faculdade de Medicina da USP, São Paulo, Brazil; 4Nelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, New York, USA; 5H. John Heinz III School for Public Policy and Management, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA 

[Citation in PubMed] [Related Articles

Abstract
To investigate the potential local health benefits of adopting greenhouse gas (GHG) mitigation policies, we develop scenarios of GHG mitigation for México City, México; Santiago, Chile; São Paulo, Brazil; and New York, New York, USA using air pollution health impact factors appropriate to each city. We estimate that the adoption of readily available technologies to lessen fossil fuel emissions over the next two decades in these four cities alone will reduce particulate matter and ozone and avoid approximately 64,000 (95% confidence interval [CI] 18,000-116,000) premature deaths (including infant deaths), 65,000 (95% CI 22,000-108,000) chronic bronchitis cases, and 46 million (95% CI 35-58 million) person-days of work loss or other restricted activity. These findings illustrate that GHG mitigation can provide considerable local air pollution-related public health benefits to countries that choose to abate GHG emissions by reducing fossil fuel combustion. Key words: air pollution, climate policy, greenhouse gases mitigation, morbidity, mortality, ozone, particulate matter, public health. -- Environ Health Perspect 109(suppl 3):419-425 (2001). 

http://ehpnet1.niehs.nih.gov/docs/2001/suppl-3/419-425cifuentes/abstract.html


Address correspondence to D. Davis, Carnegie Mellon University, 5000 Forbes Ave., Pittsburgh, PA 15213 USA. Telephone: (412) 268-5495. Fax: (412) 268-5337. E-mail: davis@andrew.cmu.edu

This work was funded by the W. Alton Jones Foundation, the Rockefeller Family Fund, the U.S. Department of Energy, the U.S. EPA (Integrated Environmental Strategies Program and (Integrated Assessment and NYU-EPA PM center grant), the Latin America Program of the World Bank, the National Ministry of Health, México, Fondecyt, Chile, the Center for Integrated Study of the Human Dimensions of Global Change, a joint creation of the National Science Foundation (SBR-9521914) and Carnegie Mellon University, and a National Institute of Environmental Health Sciences center grant (ES00260) to the New York University School of Medicine. Part of this research was developed under the International Co-Control Benefits Analysis Program, which is managed for the U.S. EPA by the National Renewable Energy Laboratory (http://www.nrel.gov/icap). 

Received 20 March 2001; accepted 25 April 2001. 

A broad-ranging and lively debate is under way about the long-term consequences of greenhouse gas (GHG)-emitting activities, such as fossil fuel combustion, for global climate change. Although it is generally understood that policies to reduce GHG emissions can also have near-term positive and negative ancillary side effects on public health, ecosystems, land use, and materials, these side effects have not been well characterized or integrated into policy analyses of mitigation (1). This article assesses near-term public health consequences of reductions in ambient concentrations of particulate matter (PM) and ozone (O3) associated with policies to reduce GHG emissions.

The approach used in this work parallels that of other recent national and regional assessments in which estimates of public health impacts of air pollution are derived from epidemiology-based concentration-
response functions. For example, Künzli et al. (2) relied on established coefficients of changes in health outcomes associated with increments of air pollution to estimate the impact of outdoor (total) and traffic-related air pollution on morbidity and mortality in Austria, France, and Switzerland. Air pollution was found to be associated with 6% of total mortality, or more than 40,000 attributable cases per year, with about half the mortalities linked to traffic-related emissions. Hall et al. (3) employed air pollutant mapping for the South Coast Basin of California and estimated that attaining ambient air pollution standards might save 1,600 lives per year in the region. The U.S. Environmental Protection Agency (U.S. EPA) employed a similar approach to assess the benefits of the U.S. Clean Air Act over its first two decades of application (4) and over the next two decades (5). The potential annual benefits from GHG mitigation options in the United States include thousands of avoided deaths and up to 520,000 work loss days that would result from the adoption of policies that target reductions in both air pollution and GHG emissions (6). Preliminary national assessments for Hungary and Canada have also suggested that substantial numbers of lives can be saved, chiefly from declines in mortality associated with fine particle reductions resulting from increased energy efficiency (7,8).

The Working Group on Fossil Fuels produced a global assessment that calculated the consequences of continuing energy policies that rely on customary practices, called business as usual (BAU), in 2010 and 2020. This study assessed the range of avoidable deaths solely from projected changes in PM that could arise between 2000 and 2020 under current policies and under the scenario proposed by the European Union in 1995 (9,10). On the basis of the estimated changes in PM and associated reductions in mortality, the report predicted that 700,000 avoidable deaths (90% confidence interval [CI] 385,000-1,034,000) will occur annually by 2020 under the BAU forecasts when compared with the climate policy scenario. As a first approximation, the cumulative impact from 2000 to 2020 on public health related to the difference in PM exposure could total 8 million deaths globally (90% CI 4.4-11.9 million). Thus, energy policies have significant impacts on air pollution and associated public health effects.

Scenario Development

As part of a collaborative project to promote consideration of public health impacts in the development of GHG mitigation policies in large cities today, this article develops scenarios that estimate the cumulative public health impacts of reducing GHG emissions from 2000 to 2020 in four cities: México City, México; São Paulo, Brazil; Santiago, Chile; and New York, New York. Using information from the published scientific literature, including those generated by local studies in each of these cities, we estimate what the adoption of climate policies would mean for public health by 2020 based on existing transportation and energy technologies that reduce the carbon intensity of fuels. For the four cities analyzed we estimate the baseline change in air pollutants associated with the adoption of energy efficiency and climate policies (CP) intended to reduce GHG emissions during the next 20 years. The CP scenario we apply to each city considers the attendant impact of GHG mitigation measures on the emissions of primary pollutants and consequent impacts on ambient concentrations of secondary pollutants. The scenarios used in this article are based largely upon a recent estimate of the potential reductions in PM and O3 ambient concentrations that have been estimated as achievable in Chile through the use of readily available technologies to mitigate GHG emissions in energy, transport, residential, and industrial sectors (11). This Chilean study shows that the adoption of energy efficiency and fuel substitution measures in transportation, energy, residences, and industry can lower GHG emissions in 2020 by approximately 13% with respect to the BAU case, at little or no cost.

The associated reductions in ambient concentrations of PM less than 10 µm in diameter (PM10) and O3 are approximately 10% of the projected baseline levels in 2020 and occur gradually throughout the two decades. These results agree with another study for Chile developed independently by the Organisation for Economic Co-operation and Development (12). On the basis of these results, we compute the benefits associated with a 10% reduction in PM and O3 that might be associated with climate change policies in each of these megacities. Although we recognize that other air pollutants may also affect human health, we consider only PM and O3 in this analysis. These two presently have the best-documented health effects across a wide range of health outcomes and are pollutants that represent, respectively, the particulate and the gaseous components of air pollution. Therefore, although conservative in that only two pollutants are considered, this analysis does consider the breadth of types of air pollution and health effect changes that would result from GHG mitigation measures.

The magnitude and scale of potential benefits of GHG mitigation will vary with the stringency of existing and proposed regulations (13). Where baseline conditions include relatively high ambient levels of pollution and unsophisticated technology, as with many rapidly developing countries such as Chile, México, and Brazil, the potential benefits of reducing emissions will likely be much larger than where baseline conditions already include fairly strict regulatory controls and advanced systems. Mitigation policies in cities that have little regulatory control will have a greater absolute impact than those in areas with well-established controls in place. To develop the scenarios in this analysis, we made a number of simplifying assumptions. We assumed that the fuel and technology mixes in the Latin American cities we assessed here were similar. Although São Paulo relied on ethanol fuels until the mid-1990s, that fuel is not expected to play a major role in the future. On the basis of recent trend information, we assumed that the concentrations of both PM10 and O3 would remain constant in these cities for the baseline scenarios. For Santiago, where progress is being made in the reduction of PM10, we assumed a reduction of 3% per year in the concentrations of PM10. Applying the 10% reduction to the projected concentrations for 2020 for México City, São Paulo, and Santiago, respectively, we project reductions of 6.4, 5.3, and 4.5 µg/m3 in the annual average of PM10, and 11.4, 6.5, and 4.9 ppb in the annual average of daily 1-hr maximum O3 by 2020.

In the analysis of air pollution-related impacts associated with GHG mitigation for New York City, a 10% reduction in O3 and PM10 from present baseline levels amounts to changes in the annual average concentrations of 3.9 ppb daily 1-hr maximum O3 and 2.2 µg/m3 annual average PM10. This assumed GHG-associated reduction in air pollution compares well with the only estimate that has been made to date regarding potential reductions that could arise from GHG mitigation in the United States. Abt Associates (6) recently estimated for the U.S. EPA that a GHG policy of applying a fee of $56/ton of carbon emitted would be associated with a reduction of between 0.4 and 2.7 µg/m3 PM2.5 in the Midwest/Northeastern United States (or about 0.6 to 3.9 µm/m3 PM10, assuming 70% is PM2.5) when compared with various baseline emissions scenarios. (PM2.5 is the mass of suspended particles less than 2.5 µm in aerodynamic diameter that can penetrate to the deepest recesses of the lung.) Thus, although New York City is very different from Santiago, the assumption of a 10% reduction from present PM10 and O3 levels in New York City appears reasonable. This is because this assumption is consistent with co-pollutant reductions previously projected to be associated with potential GHG mitigation measures in this region of the United States.

While the reductions in pollutant concentrations estimated here are similar between New York City and the Latin American cities, it must be noted that they might arise from very different policies. For developing countries, which are not required to abate GHGs under the Kyoto Protocol, the reductions stem from nonpositive cost measures of energy efficiency and fuel substitution, whereas for the United States, which is supposed to abate GHG emissions under the Kyoto Protocol, the reductions might result from the application of a carbon tax or other policies.

Health Effects Estimation Methods

To develop estimates of public health impacts in the cities of interest over the next two decades, we relied on published studies on air pollution and health, using concentration-response (C-R) coefficients derived from studies conducted in these or similar cities whenever possible. Table 1 shows a list of end points that have been associated with air pollution. The left side of the table displays effects associated with air pollution in numerous cities in more than 20 countries across the world; these effects are used extensively in standard setting (4,5,14). The effects in the right side of the table have been observed in some cities but have not yet been replicated in many locations. Assessments of air pollution-related health effects are based almost exclusively upon epidemiologic studies, which are corroborated by a body of knowledge from controlled human and animal studies (5). Most of the recent studies linking air pollution and health have applied multivariate methods, such as Poisson models, that address major potential confounders (15). In such models the expected value of the number of health effects is modeled as an exponential function of the explanatory variables, and the change in the number of health effects, J, when ambient concentrations of pollutant, P, change by Uppercase deltaCP, is given by

Uppercase deltaEJP = [exp(ßJP · Uppercase deltaCP) - 1] · PopJ · BRJ0.

ßJP is often referred to as the C-R coefficient of end point, J, associated to pollutant P. BRJ0 is the base rate of effects, J, in the affected population PopJ. For example, BRJ0 might be the number of deaths per 100,000 infants less than 1 year of age during a baseline year. However, it is important to note that the affected population is not necessarily the whole population of a city. It can be separated by age groups (e.g., infants, adults, elder) or by health conditions (e.g., asthmatic population) among many possible divisions.

Table 1. Scope of human health effects of air pollution.a

Quantifiable health effects Suspected health effects
Mortality (elder) Induction of asthma 
Mortality (infant) Fetus/child developmental
   effects
Neonatal mortality Increased airway 
   responsiveness
Bronchitis: chronic Nonbronchitis chronic 
 and acute  respiratory diseases
Increased asthma attacks Cancer
Respiratory hospital  Lung cancer
 admissions  
Cardiovascular hospital  Behavioral effects 
 admissions  (e.g., learning disabilities)
Emergency room visits  Neurologic disorders
 for asthma  
Lower respiratory illness Exacerbation of allergies
Upper respiratory illness  Altered host defense 
   mechanisms (e.g., 
   increased shortness of 
   breath susceptibility to 
   respiratory infection)
Respiratory symptoms Respiratory cell damage
Days of work loss Decreased time to onset 
   of angina
Moderate or worse  Morphologic changes in 
 asthma status  the lung
Days with restricted  Cardiovascular arrhythmia
 activity  

aAdapted from U.S. EPA (5).

Because ßJP is small, the previous equation can be linearized and expressed in the following terms:
 
 


models for the expected value of the number of health effects


 






where Pop is the total population of an area of analysis and IFJP is the health impact factor of pollutant P for end point J. It encompasses the relative risk, the base rate of the effect, and the relative size of the exposed population as a fraction of the total population. By expressing it this way, it is straightforward to compare the relative impact of pollution across different populations, and to compute the changes in health effects from the changes in concentrations and total population of a given city.

An important decision in the estimation of pollution effects involves the selection of pollutants for analysis. Incremental changes in mortality and morbidity associated with changes in exposures to PM have been documented extensively. A number of other common air pollutants, including sulfur dioxide, carbon monoxide, nitrogen oxides (NOx), and O3 have also been linked with various health effects. Inclusion of several pollutants in a single analysis simultaneously can lead to overestimation of the total effects if the C-R coefficients for each pollutant have been derived independently and the effects are added up later. Conversely, consideration of only one pollutant (PM10, for example) to estimate the effects can underestimate the total air pollution effects, as several analyses show that the total risk of air pollution increases when more pollutants in addition to PM10, such as O3 and nitrogen dioxide (NO2), are considered (16,17). In this analysis we considered two pollutants that have shown consistent and relatively independent associations with an array of adverse health effects: PM and O3.

Ideally, the estimation of the change in health effects associated with concentrations in a given city should be based on studies conducted locally. However, local studies are not available for every health effect in every city. Therefore, we also use studies from other similar places, as available. For morbidity, C-R functions were derived from pooled estimates from the international literature when more than three studies were available. Random effects models were used to obtain a summary measure in this meta-analysis (18). For the case of O3, studies taking into account the effects of PM10 simultaneously were employed when available. Latin American studies were preferred for the cities in that region. Regionally relevant information was available for the acute effects of PM on mortality for each of the cities. For example, whereas New York City infant mortality and hospital admissions effects were estimated using U.S.-based studies, the Latin American cities' pollution effect on infant mortality was derived from México City (19), child medical visits from Santiago (20), and hospital admissions from São Paulo (21).

The effects of PM exposure on mortality have been derived both from time-series studies that evaluate the effect of several days of elevated or acute exposures on daily mortality and from cohort studies that evaluate the annual changes in mortality or morbidity associated with long-term, chronic exposures. Because the estimates from these two types of studies focus on different time frames, we used both types to indicate the likely upper- and lower-bound effects on mortality. Two main cohort studies of the general population have reported different central effect estimates, although their CIs overlap. We used the Pope et al. (22) and the Dockery et al. (23) studies to derive the central and high estimates of mortality, respectively. A recent reanalysis of these studies has been conducted by the Health Effects Institute and has confirmed their results (24). The lower bound of mortality effects were obtained from time-series studies, as shown in Table 2. Some have raised the issue that these studies may reflect life shortening of only a few days or weeks [sometimes referred to as "harvesting" (25)], but recent analyses have not borne out this assertion (26-28). The effects of O3 on mortality in the Latin American cities were obtained from a meta-analysis of several studies.

Table 2. Studies considered in the analysis of the mortality effects of PM10 for México City, São Paulo, and Santiago.

All ages mortality City
Age group 
Relative risk for 10 µg/m3 increase
in PM10 (95% CI) (percent)
Reference

  Low estimate
México City
All
1.2 (1.1-1.2)
(33)
 
São Paulo
All
0.85 (0.46-1.2) 
(34,35)
 
Santiago
All
0.7 (0.3-1.0)
(16)a
  Mid estimate
All cities
> 30 years
3.5 (1.9-5.2) 
(22)a
  High estimate
All cities
> 25 years
6.8 (2.7-11.4)
(23)a
Infant mortality
All cities
< 1 year
4.0 (1.6-6.5)
(19)

aRelative risks were multiplied by 0.55 when the pollutant in the original study was PM2.5.

In New York, the health effects associated with the GHG mitigation-induced air pollution decreases were based largely on the C-R coefficients derived from the published literature for New York State by the Empire State Electric Energy Research Corporation (ESEERCO) as part of the New York State Environmental Externalities Cost Study (29). In some cases, however, alternative study results were used to define the bounds, such as in the case of PM10-associated mortality. In this case, as for the Latin American cities, the Pope et al. study (22) of the effects of chronic PM exposure was used as the central estimate, the Dockery et al. study (23) was used to estimate the upper bound, and the results of a time-series PM study of the effects of acute PM exposure were used for the lower bound (as derived from the ESEERCO report). In addition, the ESEERCO C-R coefficients were updated with newer studies as appropriate, and studies conducted in or near New York State were chosen when available.

For each end point, we derived health impact factors (as defined above) specific for each city, as presented in Tables 3-5. Although some of the relative risks are similar for the cities, the impact factors differ because the population distribution of those affected differs between cities, as does the baseline rate of hospitalization and other end points. For instance, infant mortality impacts are higher in Latin American cities, in part because they have higher baseline rates. Conversely, the impact factors for adult health outcomes (e.g., work loss days and chronic bronchitis) are usually higher per million people for New York City than for the Latin American cities, largely due to the higher percentage of more frail, older individuals in this more-developed, lower birth rate city. In addition, this analysis assumes a higher percentage of the PM10 is PM2.5 in New York City versus the developing nation cities (70% vs 55%), which increases the impacts per µg/m3 of PM10 reduction in New York City versus the other cities. To estimate the total health effects avoided during the next two decades, we applied the impact factors to the projected population and concentration changes, making the simplifying assumption that the current health conditions in these cities would prevail and that population would increase according to official projections, except in New York City, where a stable population size was assumed.

Table 3. O3 and PM10 health impact factors and CIs for New York City.

 
Health impact factor per million inhabitants
 
 
 
Health effect outcome
Mid
95% CI
Reference

Ozone impacts (effects per part per billion of annual average daily 1-hr maximum ozone)  
  Acute mortality 
1.2
(0.0-2.4)
(36)
  Acute respiratory hospital admissions
5
(3-7)
(37)
  Acute emergency department visits
40
(25-55)
(38)
  Acute asthma attacks
1,005
(570-2,747)
(39)
  Acute restricted activity days
17,000
(7,000-27,000)
(40,41)
  Acute respiratory symptom days
50,000
(26,000-78,000)
(42)
PM10 impacts (effects per microgram per cubic meter of PM10)
  Acute and chronic infant mortality
0.21
(0.1-0.3)
(43)
  Acute and chronic adult mortality 
33
(8-52)
(22) 
  Acute respiratory hospital admissions
12
(7-17)
(44)
  Chronic adult bronchitis
39
(19-59)
(45)
  Acute bronchitis in children
53
(26-78)
(46)
  Acute emergency department visits
94
(55-130)
(38)
  Acute asthma attacks
774
(446-2,589)
(39) 
  Acute work loss days
5,300
(2,700-8,300)
(47)
  Acute restricted activity days
14,900
(7,616-23,509)
(48)
  Acute respiratory symptom days
170,000
(81,000-259,000)
(42)



Table 4. PM10 health impact factors (with 95% CIs) developed for México City, São Paulo, and Santiago.a

México City
São Paulo
Santiago



End point
Age group (years)
Mid
95% CI
Mid
95% CI
Mid
95% CI
References

Mortality effects                
  Mortality
Allb
21
(7-41)
20
(2-39)
12
(2-23)
See Table 2
  Infant mortality
< 1 
2.2
(0.9-3.6)
1.2
(0.5-2.0)
0.9
(0.4-1.5)
See Table 2
Chronic morbidity effects                
  Chronic bronchitis
> 30 
26
25.6
21.1
(8-43)
20.9
(6-36)
(49)
Hospital admissions                
  Cardiovascular causes
All
2.4
(2-3)
2.4
(2-3)
2.4
(2-3)
Pooled from Los Angeles (50), Ontario  (51), Detroit (52), Michigan (53), Chicago (54)
  Respiratory causes
All
5.7
(4-8)
5.7
(4-8)
5.7
(4-8)
Pooled from California (55), Ontario (51), Paris (56), London (57),  Amsterdam (58), Rotterdam (58),  Cleveland (59), Buffalo (37), New  York (37), Ontario (60), Milan (61),  Los Angeles (50)
  Children: all causes
< 13 
3.2
(2-5)
8.2
(4-12)
8.2
(4-12)
São Paulo (21)
Other hospital visits                
  Emergency room visits
All
141
(0-351)
93
(0-232)
93
(0-232)
Pooled from London (62), México (63), 
               
 Quebec (64), Steubenville (65)
  Children: medical visits
3-15 
63
(14-112)
155
(34-275)
83
(18-147)
Santiago (20)
Morbidity effects                
  Asthma attacks
All
668
(161-1,175)
668
(161-1,175)
668
(161-1,175)
(39)
  Children: acute bronchitis
8-12 
65
(0-145)
64
(0-143)
62
(0-138)
(46)
Restricted activity                
  Work loss days
18-65 
3,655
(3,095-4,216)
3,965
(3,357-4,573)
3,657
(3,096-4,217)
(47)
  Restricted activity days
18-65 
10,539
(9,287-11,792)
11,431
(10,073-12,790)
10,543
(9,291-11,796)
(47)

aEffects per million people per microgram per cubic meter PM10. bThe age groups considered vary according to the estimate (see Table 2 for details).



Table 5. Ozone health impact factors and 95% CIs developed for México City, São Paulo, and Santiago.a

México City
São Paulo
Santiago



End point
Age group (years)
Mid
95% CI
Mid
95% CI
Mid
95% CI
References

Acute mortality                
  Total
All
1.9
(1.0-2.7)
1.8 
(1.0-2.7)
1.0
(0.2-1.7)
México City and São Paulo: pooled from London (66), México (67), México (33), Chicago (68), Phila delphia (69,70), Amsterdam (71), European cities (72), Rotterdam (73). Santiago: summer (16)
Hospital admissions                
  Respiratory causes
All
15
(2-29)
15
(2-29)
15
(2-29)
Pooled from Buffalo (37), New York (37), Ontario (60)
  All causes: children
< 5 
0.29
(0.03-0.55)
0.65
(0.07-1.23)
0.50
(0.05-0.94)
Brazil (74)
Other hospital visits                
  ERV for RSP causes
All
144
(76-212)
95
(50-140)
144
(76-212)
Pooled from Montreal (64), México (75), Ontario (17)
Morbidity effects                
  Asthma attacks
All
1,140
(0-2,745)
1,140
(0-2,745)
1,140
(0-2,745)
(46)
  Restricted activity days
Adults
11,781
(8,036-13,678)
12,779
(8,716-14,835)
11,786
(8,039-13,683)
 

ERV for RSP, emergency room visits for respiratory causes.
aEffects per million people per part per billion per cubic meter annual average daily 1-hr maximum O3.

Results

Tables 6 and 7 present the health effects estimated to be avoided in the four cities for the period 2000-2020 if modest GHG mitigation measures are initiated now, due to expected reductions in concentrations of PM and O3, respectively. Figure 1 shows the total effects due to PM and O3 reductions for all four cities combined. Not all end points could be evaluated for all cities, as relevant studies were not always available for every outcome for every city. Therefore, some of the estimations presented here are likely to be underestimates.

Table 6. Health effects avoided from 2000 to 2020 in the four cities due to PM10 reductions if GHG mitigation measures are taken.

México City
São Paulo
Santiago
New York
   



End point
Age group (years) 
Mid
95% CI
Mid
95% CI
Mid
95% CI
Mid 
95% CI

Mortality effects                  
  Mortality
All
29,055
(9,265-
56,293)
11,225
(1,173-
21,749)
3,960
(801-
7,673)
8,785
(2,130-
13,842)
  Infant mortality
< 1
3,065
(1,187-
4,944)
701
(271-
1,130)
320
(124-
516)
56
(43-
75)
Chronic morbidity effects
  Chronic bronchitis
> 30
35,353
(10,904-
59,803)
11,899
(3,670-
20,129)
7,087
(2,186-
11,989)
10,382
(5,058-
15,706)
Hospital admissions
  Cardiovascular causes
All
3,341
(2,339-
4,344)
1,365
(956-
1,775)
819
(575-
1,062)
 
  Respiratory causes
All
7,894
(5,026-
10,763)
3,226
(2,054-
4,398)
1,934
(1,231-
2,637)
3,194
(1,863-
4,525)
  Children: all causes
< 13 
4,475
(2,282-
6,668)
4,638
(2,365-
6,911)
2,788
(1,422-
4,154)
 
Other hospital visits
  Emergency room visits
All
195,355
(0-
484,682)
52,756
(0 -
130,890)
31,631
(0 -
78,478)
25,023
(14,641-
34,606)
  Medical visits
3-
15
87,064
(19,217-
154,912)
87,377
(19,286-
155,468)
28,054
(6,192-
49,916)
(0-
0)
Morbidity effects
  Asthma attacks
All
923,315
(222,624-
1,624,005)
377,312
(90,975-
663,649)
226,226
(54,546-
397,906)
205,988
(118,839-
689,268)
  Acute bronchitis
8-
12
89,897
(0-
200,805)
36,157
(0 -
80,764)
20,876
(0 -
46,631)
14,055
(6,838-
20,893)
Restricted activity
  Work loss days
18-
65 
5,051,218
(4,276,788-
5,825,648)
2,238,907
(1,895,648-
2,582,167)
1,238,111
(1,048,289-
1,427,933)
1,404,099
(717,650-
2,215,355)
  Restricted activity days 
18-
65 
14,563,826
(12,833,091-
16,294,560)
6,455,286
(5,688,153-
7,222,418)
3,569,759
(3,145,537-
3,993,982)
3,966,380
(2,027,261-
6,258,066)



Table 7. Health effects avoided from 2000 to 2020 in the four cities due to ozone reductions if GHG mitigation measures are taken.

   
México City
São Paulo
Santiago
New York
   



End point
Age group (years)
Mid
95% CI
Mid
95% CI
Mid
95% CI
Mid
95% CI

Acute mortality                  
  Total
All
4,610
(2,500-
6,720)
1,256
(681-
1,831)
293
(54-
533)
566
(0-
1,133)
Hospital admissions                  
  Respiratory causes
All
37,964
(4,746-
71,183)
10,588
(1,324-
19,853)
4,738
(592-
8,884)
2,360
(1,463-
3,256)
  All causes 
< 5
721
(79-
1,363)
447
(49-
846)
153
(17-
289)
   
Other hospital visits                  
  ERV for RSP causes
All
354,005
(186,495-
521,515)
65,245
(34,372-
96,119)
44,183
(23,276-
65,090)
18,876
(11,798-
25,955)
Morbidity effects                  
  Asthma attacks
All
2,800,570
(0-
6,744,230)
781,070
(0-
1,880,943)
349,538
(0-
841,745)
474,260
(268,747-
1,296,309)
  Restricted activity days
Adults
28,942,806
(19,742,221-
33,601,432)
8,755,334
(5,972,114-
10,164,590)
3,613,755
(2,464,984-
4,195,424)
8,022,300
(30,303,300-
12,741,300)

Figure 1

Figure 1. Health effects avoided from 2000 to 2020 in the four cities analyzed if GHG mitigation measures are taken.
For the period analyzed, nearly 64,000 (95% CI 18,000-116,000) premature deaths associated with air pollution could be avoided if policies aimed at achieving modest reductions in GHG emissions are undertaken now. We also estimate that at least 65,000 (95% CI 22,000-108,000) new cases of chronic bronchitis; 91,000 (95% CI 28,000-153,000) hospital admissions; and 787,000 (95% CI 136,000-1,430,000) emergency room visits could be avoided. Other effects may appear less important, but their numbers are quite high. We predict that 6.1 million (95% CI 0.49-14.1 million) asthma attacks can be avoided, as well 37 million (95% CI 27-47 million) work loss days or other days with restricted activity.

The effects in children are also important to note. Premature deaths of infants less than 1 year of age (including neonatal mortality) that can be avoided amount to 4,100 (95% CI 1,600-6,700). In addition, more than 161,000 (95% CI 0-350,000) cases of acute bronchitis in children 8-12 years of age as well as 202,000 (95% CI 45,000-360,000) medical visits of children 3-15 years of age could be avoided. (This last effect was evaluated only in the Latin American cities.)

Discussion

Analyzing the total burden on human health from ambient air pollution in a community remains challenging, given the uneven nature of information on which such assessments must draw, the absence of information on many key pollutants, and the wide range of uncertainties characterizing many parts of the process. Because we have data from the cities reviewed here on the entire age range of the population and a broad range of effects that could occur throughout this range, this analysis provides a more robust assessment than past global efforts (10). Still, there is much that is not addressed in this work, including impacts on ecosystems, water supply and quality, agriculture, and materials damage.

We believe that our analysis is conservative for various reasons. First, we assumed no major changes in technologies for transport, energy, and commerce in the next two decades. Some air pollutants (such as O3, some aromatic hydrocarbons, and NO2) continue to increase in many metropolitan regions; their full impact is not assessed in this analysis. In addition, we could not include estimates of synergistic effects between various air pollutants, or with cofactors such as pollen and other allergens. New studies have indicated that synergies can occur between air pollutants and allergens. Thus, for example, British analyses show that physician visits for asthma and allergic rhinitis are increased more than additively when both pollen and air pollution levels are elevated (30). We also did not consider effects tied with cancer (31) and other diseases linked with exposures to pollution and other airborne toxics, which are not usually monitored and can be quite high in rapidly developing areas (32).

The rapid pace of urbanization globally means that more people are living in large cities than at any point in human history. Policies that increase energy efficiency and promote less carbon-intensive fuels can yield a broad array of benefits by simultaneously improving local and regional air pollution and reducing the long-term buildup of GHG. Given the current and projected patterns of population growth and air pollution concentrations, the cumulative potential impact on public health from fossil fuels for the next two decades is quite high for any of the cities analyzed. Part of this burden can be avoided if GHG abatement policies to reduce the net use of fossil fuels are adopted. For Santiago and the other cities, the adoption of currently available technologies in energy, transport, residences, and industry can reduce population exposure to air pollution by at least 10% by 2020, yielding the associated public health benefits we have presented. Similar types of health impact reductions are expected to occur in other developing world cities if GHG emissions mitigation policies are also implemented in those cities.

This current collaborative analysis stems from an effort to integrate into the public discussion of GHG mitigation policies a consideration of what these policies might mean for public health in the nearer term. We fully recognize that population patterns can be changed by events not integrated into this assessment. We also are not unaware of promising technologies, such as fuel cells for energy production and transportation applications, that might substantially alter air pollutant emissions in the future. The estimates developed here are offered to illustrate the potential scale and scope of impacts. A fuller accounting would likely show still greater public health and natural resource benefits than this preliminary assessment.

Conclusion

The estimates offered here are presented for three purposes: to stimulate discussion of the full range of potential impacts of changes in future patterns of air pollution in developed and developing countries; to bring the subject of public health benefits to the attention of those who are formulating public policy regarding GHG mitigation; and to encourage additional research on this topic. The preliminary results in this work indicate that policies aimed at mitigating GHG emissions can provide a broad range of more immediate air pollution benefits to public health in the countries that implement these GHG mitigation measures. Conversely, not acting or postponing actions to reduce GHG emissions will fail to achieve the health benefits we present in this analysis.

The estimates of the potential public health benefits from the adoption of GHG mitigation policies offered in this paper were developed opportunistically, incorporating results from a variety of studies conducted for different purposes. While it must be acknowledged that there is still much that remains to be learned about the intricacies of climate change and the respective (and potentially interactive) roles of the various air pollutants, the numbers developed for these four cities illustrate the magnitude and scale of the air pollution impacts that may be averted by implementing GHG mitigation measures, according to current understanding. As pressures mount for actions to be taken to reduce GHG emissions, decisions being made in the next decade will affect the forms of energy production and transportation systems that will fuel this century in many regions. Further, efforts to promote a sounder accounting of how these technologies will affect public health must be encouraged. The failure to provide a fuller tally of potential health damages tied with air pollution in the discussions of GHG mitigation policies not only limits the utility of those discussions but also fails to meet a basic human concern. People care greatly about their health and the health of their children. Decision makers need to be well informed about the extent to which global climate policies adopted today can be expected to affect public health in both the near and long term.
 
 


REFERENCES AND NOTES


 






1. Davis DL, Krupnick A, McGlynn G. Ancillary benefits and costs of greenhouse gas mitigation: an overview. In: Ancillary Benefits and Costs of Greenhouse Gas Mitigation. Proceedings of an IPCC Co-sponsored workshop, 27-29 March 2000, Washington, DC. Paris:Organisation for Economic Co-operation and Development, 2000;9-49.

2. Künzli N, Kaiser R, Medina S, Studnicka M, Chanel O, Filliger P, Herry M, Horak FJ, Puybonnieux-Texier V, Quenel P, et al. Public-health impact of outdoor and traffic-related air pollution: a European assessment. Lancet 356:795-801 (2000).

3. Hall JV, Winer AM, Kleinman MT, Lurmann FW, Brajer V, Colome SD. Valuing the health benefits of clean air. Science 255:812-817 (1992).

4. U.S. EPA. The Benefits and Costs of the Clean Air Act, 1970 to 1990. Report Prepared for the U.S. Congress. Washington, DC:U.S. Environmental Protection Agency, 1997.

5. U.S. EPA. The Benefits and Costs of the Clean Air Act, 1990 to 2010. EPA-410-R-99-001. Washington, DC:U.S. Environmental Protection Agency, 1999.

6. Abt Associates Inc. Co-Control Benefits of Greenhouse Gas Control Policies. Prepared for the U.S. Environmental Protection Agency. Bethesda, MD:Abt Associates Inc, 1999.

7. Aunan K, Aaheim HA, Seip HM. Reduced damage to health and environment from energy saving in Hungary. Ancillary Benefits and Costs of Greenhouse Gas Mitigation. In: Proceedings of an IPCC Co-sponsored workshop, 27-29 March 2000, Washington, DC. Paris:Organisation for Economic Co-operation and Development, 2000;237-261.

8. Last J, Trouton K, Pengelly D. Taking Our Breath Away. The Health Effects of Air Pollution and Climate Change. Vancouver, BC, Canada:David Suzuki Foundation, 1998;51.

9. Davis D. The hidden benefits of climate policy: reducing fossil fuel use saves lives now. Environmental Health Notes. Washington, DC:World Resources Institute, 1997.

10. Working Group on Public Health and Fossil-fuel Combustion. Short-term improvements in public health from global-climate policies on fossil-fuel combustion: an interim report. Lancet 350:1341-1349 (1997).

11. Cifuentes LA, Sauma E, Jorquera H, Soto F. Preliminary estimation of the potential ancillary benefits for Chile. In: Ancillary Benefits and Costs of Greenhouse Gas Mitigation. Proceedings of an IPCC Co-sponsored workshop, 27-29 March 2000, Washington, DC. Paris:Organisation for Economic Co-operation and Development, 2000;237-261.

12. Dessus S, O'Connor D. Climate Policy without Tears: CGE-Based Ancillary Benefits Estimates for Chile. Technical Paper no 156. Paris:Organisation for Economic Co-operation and Development, 1999.

13. Morgenstern R. Baseline issues in the estimation of the ancillary benefits of greenhouse gas mitigation policies. In: Ancillary Benefits and Costs of Greenhouse Gas Mitigation. Proceedings of an IPCC Co-sponsored workshop, 27-29 March 2000, Washington, DC. Paris:Organisation for Economic Co-operation and Development, 2000;95-122.

14. U.S. EPA. Regulatory Impact Analysis for the Particulate Matter and Ozone National Ambient Air Quality Standards and Proposed Regional Haze Rule. Research Triangle Park, NC:U.S. Environmental Protection Agency, 1997.

15. Pope CA III. Epidemiology of fine particulate air pollution and human health. Environ Health Perspect 108:713-723 (2000).

16. Cifuentes L, Lave L, Vega J, Kopfer K. Effect of the fine fraction of particulate matter vs the coarse mass and other pollutants on daily mortality in Santiago, Chile. J Air Waste Manag Assoc 50:1287-1298 (2000).

17. Burnett T, Cakmak S. The effect of the urban ambient air pollution mix on daily mortality rates in 11 Canadian cities. Rev Can Santé Publique 89:152-156 (1998).

18. Blettner M, Sauerbrei W, Schlehofer B, Scheuchenpflug T, Friedenreich C. Traditional rewiews, meta-analysis and pooled analysis in epidemiology. Int J Epidemiol 28:1-9 (1999).

19. Loomis D, Castillejos M, Gold D, McDonnell W, Borja-Aburto V. Air pollution and infant mortality in México City. Epidemiology 10:118-123 (1999).

20. Ostro BD, Eskeland GS, Sanchez JM, Feyzioglu T. Air pollution and health effects: a study of medical visits among children in Santiago, Chile. Environ Health Perspect 107:69-73 (1999).

21. Braga A, Conceicao G, Pereira L, Kishi H, Pereira J, Andrade M. Air pollution and pediatric hospital admissions in Sao Paulo, Brazil. J Environ Med 1:95-102 (1999).

22. Pope CA III, Thun MJ, Nambordini MM, Dockery D, Evans JS, Speizer FE, Heath CW Jr. Particulate air pollution as a predictor of mortality in a prospective study of U.S. adults. Am J Respir Crit Care Med 151:669-674 (1995).

23. Dockery DW, Pope CA III, Xu X, Spengler JD, Ware JH, Fay ME, Ferris BG Jr, Speizer FE. An association between air pollution and mortality in six U.S. Cities. N Engl J Med 329:1753-1759 (1993).

24. Krewski D, Burnett RT, Goldberg MS, Hoover K, Siemiatycki J, Jerret M, Abrahamowicz M, White WH. Reanalysis of the Harvard Six Cities Study and the American Cancer Society Study of Particulate Air Pollution and Mortality Special Report. Cambridge, MA:Health Effects Institute, 2000.

25. McMichael AJ, Anderson HR, Brunekreef B, Cohen A. Inappropriate use of daily mortality analyses to estimate longer-term mortality effects of air pollution. Int J Epidemiol 27:450-453 (1998).

26. Zeger SL, Dominici F, Samet J. Harvesting-resistant estimates of air pollution effects on mortality. Epidemiology 10:171-175 (1999).

27. Schwartz J. Harvesting and long term exposure effects in the relation between air pollution and mortality. Am J Epidemiol 151:440-448 (2000).

28. Schwartz J. Is there harvesting in the association of airborne particles with daily deaths and hospital admissions? Epidemiology 12:55-61 (2001).

29. Rowe RD, Lang C, Chestnut L, DA Latimer, Rae D, Bernbow S, White D. The New York Electricity Externality Study. New York:Oceana Publications, 1995.

30. Higgins BG, Francis HC, Yates C, Warburton CJ, Fletcher AM, Pickering CA, Woodcock AA. Environmental exposure to air pollution and allergens and peak flow changes. Eur Respir J 16:61-66 (2000).

31. Cohen A. Outdoor air pollution and lung cancer. Environ Health Perspect 108:743-749 (2000).

32. Suh H, Bahadori T, Vallarino J, Spengler JD. Criteria air pollutants and toxic air pollutants. Environ Health Perspect 108:625-633 (2000).

33. Borja-Aburto VH, Loomis DP, Bangdiwala SI, Shy CM, Rascon-Pacheco RA. Ozone, suspended particulates, and daily mortality in México City. Am J Epidemiol 145:258-268 (1997).

34. Saldiva P, Pope CA III, Schwartz J, Dockery DW, Lichtenfels AJ, Salge JM, Barone I, Bohm GM. Air pollution and mortality in elderly people: a time-series study in São Paulo, Brazil. Arch Environ Health 50:159-163 (1995).

35. Gouveia N, Fletcher T. Air pollution and daily mortality in Sao Paulo, Brazil: effects by cause, age and socioeconomic status. J Epidemiol Community Health 54:750-755 (2000).

36. Kinney PL, Ozkaynak H. Associations of Daily Mortality and Air Pollution in Los Angeles County. Environ Res 54:99-120 (1991).

37. Thurston GD, Ito K, Kinney PL, Lippmann M. A multi-year study of air pollution and respiratory hospital admissions in three New York State metropolitan areas: results for 1988 and 1989 summers. J Expo Anal Environ Epidemiol 2:429-450 (1992).

38. Barton D, Tets-Grimm K, Kattan M. Emergency room patterns of inner city children for asthma [Abstract]. Am Rev Respir Dis 47:A577 (1993).

39. Whittemore AS, Korn EL. Asthma and air pollution in the Los Angeles area. Am J Public Health 70:687-696 (1980).

40. Portney P, Mullahy J. Urban air quality and chronic respiratory disease. Reg Sci Urb Econ 20:407-418 (1990).

41. Ostro BD, Rothschild S. Air pollution and acute respiratory morbidity: an observational study of multiple pollutants. Environ Res 50:238-247 (1989).

42. Krupnick A, Harrington W, Ostro B. Ambient ozone and acute health effects: evidence from daily data. J Environ Econ Manag 18:1-18 (1990).

43. Woodruff TJ, Grillo J, Schoendorf KC. The relationship between selected causes of postneonatal infant mortality and particulate air pollution in the United States. Environ Health Perspect 105:608-612 (1997).

44. Pope CA III, Dockery D, Spengler JD, Raizenne ME. Respiratory health and PM10 pollution: a daily time series analysis. Am Rev Respir Dis 144:668-674 (1991).

45. Abbey DE, Petersen F, Mills PK, Beeson WL. Long term ambient concentrations of total suspended particulates, ozone and sulfur dioxide and respiratory symptoms in a non-smoking population. Arch Environ Health 48:33-46 (1993).

46. Dockery DW, Speizer FE, Stram DO, Ware JH, Spengler JD, Ferris BG Jr. Effects of inhalable particles on respiratory health of children. Am Rev Respir Dis 139:587-594 (1989).

47. Ostro BD. Air pollution and morbidity revisited: a specification test. J Environ Econ Manag 14:87-98 (1987).

48. Ostro BD. Associations between morbidity and alternative measures of particulate matter. Risk Anal 10:421-427 (1990).

49. Schwartz J. Particulate air pollution and chronic respiratory disease. Environ Res 62:7-13 (1993).

50. Linn WS, Szlachcic Y, Gong H Jr, Kinney PL, Berhane KT. Air pollution and daily hospital admissions in metropolitan Los Angeles. Environ Health Perspect 108:427-434 (2000).

51. Burnett R, Robert T, Daniel D, Krewski R, Dann T, Brook J. Associations between ambient particulate sulphate and admissions to Ontario hospitals for cardiac and respiratory diseases. Am J Epidemiol 142:15-22 (1995).

52. Schwartz J, Morris R. Air pollution and hospital admission for cardiovascular disease in Detroit, Michigan. Am J Epidemiol 142:23-35 (1995).

53. Schwartz J. Air pollution and hospital admissions for cardiovascular disease in Tucson. Epidemiol 8:371-377 (1997).

54. Morris SC. Carbon monoxide and hospital admission for congestive heart failure: evidence of an increase effect at low temperatures. Environ Health Perspect 106:649-653 (1998).

55. Abbey DE, Ostro BE, Petersen F, Burchette RJ. Chronic respiratory symptoms associated with estimated long-term ambient concentrations of fine particulates less than 2.5 microns in aerodynamic diameter (PM 2.5) and other air pollutants. J Expo Anal Environ Epidemiol 5:137-159 (1995).

56. Dab W, Medina S, Quenel P, Moullec YL, Tertre AL, Thelot B, Monteil C, Lameloise P, Pirard P, Momas I, et al. Short term respiratory health effects of ambient air pollution: results of the APHEA project in Paris. J Epidemiol Community Health 50:542-546 (1996).

57. Ponce de Leon A, Anderson HR, Bland JM, Strachan DP, Bower J. Effects of air pollution on daily hospital admissions for respiratory disease in London between 1987-88 1991-92. J Epidemiol Community Health 50:63-70 (1996).

58. Schouten J, Vonk J, Graff A. Short term effects of air pollution on emergency hospital admissions for respiratory disease: results of the APHEA project in two major cities in the Netherlands, 1977-89. J Epidemiol Community Health 50:s22-s30 (1996).

59. Schwartz J, Spix C, Touloumi G, Bacharova L, Barumamdzadeh Y, Le Tretre A, Pierkarski T, Ponce de Leon A, Ponka A, Rossi G, et al. Methodological issues in studies of air pollution and daily counts of deaths or hospital admissions. J Epidemiol Community Health 50 (suppl A):S3-S11 (1996).

60. Thurston G, Ito K, Hayes C, Bates D, Kinney P, Lippmann M. Respiratory hospital admissions and summertime haze air pollution in Toronto, Ontario: consideration of the role of acid aerosols. Environ Res 65:271-290 (1994).

61. Vigotti M. Short term effects of urban air pollution on respiratory health in Milan, Italy 1980-89. J Epidemiol Community Health 50:71-75 (1996).

62. Atkinson RW. Short-term associations between outdoor air pollution and visits to accident and emergency departments in London for respiratory complaints. Eur Respir J 13:257-265 (1999).

63. Damakosh A, Castillejos M, Bierzwinski S, Retama A, Gold D. Unpublished data.

64. Delfino R, Murphy-Moulton A, Burnett R, Brook J, Becklake M. Effects of air pollution on emergency room visits for respiratory illnesses in Montreal, Quebec. Am J Respir Crit Care Med 155:568-576 (1997).

65. Samet JM. Particulate air pollution and mortality: the Philadelphia story. Epidemiology 6:471-473 (1995).

66. Anderson HR, Ponce de León A, Bland J, Bower JS, Strachan DP. Air pollution and daily mortality in London: 1987-92. Br Med J 312:665-669 (1996).

67. Borja-Aburto VH, Castillejos M, Gold DR, Bierzwinski S, Loomis DP. Mortality and ambient fine particles in Southwest México City, 1993-1995. Environ Health Perspect 106:849-855 (1998).

68. Ito K, Thurston GD. Daily PM10/mortality associations: an investigation of at-risk subpopulations. J Expo Anal Environ Epidemiol 6:79-95 (1996).

69. Kelsall JE, Samet JS, Zeger S, Xu J. Air Pollution and mortality in Philadelphia, 1974-1988. Am J Epidemiol 146:750-762 (1997).

70. Moolgavkar SH, Luebeck EG. A critical review of the evidence on particulate air pollution and mortality. Epidemiology 7:420-428 (1996).

71. Verhoeff A, Hoek G, Schwartz J, Wijnen JV. Air pollution and daily mortality in Amsterdam. Epidemiology 7:225-230 (1996).

72. Touloumi G, Katsouyanni K, Zmirou D, Schwartz J, Spix C, de Leon AP, Tobias A, Quennel P, Rabczenko D, Bacharova L, et al. Short-term effects of ambient oxidant exposure on mortality: a combined analysis within the APHEA project. Air pollution and health: a European approach. Am J Epidemiol 146:177-185 (1997).

73. Hoek G, Schwartz J, Groot B, Eilers P. Effects of ambient particulate matter and ozone on daily mortality in Rotterdam, the Netherlands. Arch Environ Health 52:455-463 (1997).

74. Gouveia N, Fletcher T. Respiratory diseases in children and outdoor air pollution in Sao Paulo, Brazil: a time series analysis. Occup Environ Med 57:477-483 (2000).

75. Téllez-Rojo M, Romieu I, Polo-Peña M, Ruiz-Velasco S, Menesses-González F. MH-A. Efecto de la contaminación ambiental sobre las consultas por infecciones respiratorias en niños de la ciudad de México. Salud Pública Méx 39:513-522 (1997).


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