© 2003 American Public Health Association
Nino Künzli, Rob McConnell, Tracy Bastain, Andrea Hricko, Ed Avol, Frank Gilliland, and John Peters are with the Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles. David Bates is with the Departments of Medicine and Physiology, University of British Columbia, Vancouver. Fred Lurmann is with Sonoma Technology Inc, Petaluma, Calif. Correspondence: Requests for reprints should be sent to Nino Künzli, MD, PhD, Department of Preventive Medicine, Keck School of Medicine, University of Southern California, 1540 Alcazar St, CHP 236, Los Angeles, CA 90033 (e-mail: kuenzli{at}usc.edu).
Population growth and the proliferation of roadways in Southern California have facilitated a glut of mobile air pollution sources (cars and trucks), resulting in substantial atmospheric pollution. Despite successful efforts over the past 40 years to reduce pollution, an alarming set of health effects attributable to air pollution have been described in Southern California. The Childrens Health Study indicates that reduced lung function growth, increased school absences, asthma exacerbation, and new-onset asthma are occurring at current levels of air pollution, with sizable economic consequences. We describe these findings and urge a more aggressive effort to reduce air pollution exposures to protect our childrens health. Lessons from this "case study" have national implications.
ROADWAYS ARE AN IMPORTANT feature of the built environment in the United States, one that has developed as a result of massive investment and of public policy heavily influenced by private interests. Los Angeles once had a model public transit system based on an extensive and efficient network of electric trolleys. This system, along with the streetcar systems in 45 other cities, was bought and dismantled in the 1930s by National City Lines, a holding company owned by corporate partners in the automotive industry.1 In Los Angeles alone, the people who made 280 million passenger trips a year on the mass transit system were forced into other forms of transportation. The automobile controlled the future of Los Angeles. Today, a large proportion of the US population lives in heavily populated "mega-cities," such as the greater Los Angeles region, and depends on automobiles for transportation and diesel trucks and trains for transporting goods. Truck and automobile emissions are responsible for most of the air pollution in Southern California, with significant additional mobile source contributions from airports and the nations largest marine port complex. In Southern California, episodic outdoor levels of ozone (O3), particulate matter less than 10 microns in diameter (PM10), and nitrogen dioxide (NO2) historically have been among the highest in the United States, and they continue to exceed federal and state clean air guidelines.2,3 Research conducted in the 1970s and 1980s confirmed acute effects of exposure to ozone and other traffic-related pollutants.4,5 However, until recently, long-term health consequences were more uncertain, particularly among children, a population with rapidly growing lungs likely to be sensitive to the effects of air pollution.
The Childrens Health Study (CHS), begun in Southern California in 1993, is one of the largest and most comprehensive investigations of the long-term consequences of air pollution on the respiratory health of children.2,6 The purpose of this article is to summarize findings and future research strategies of the CHS and to discuss trafficrelated regulatory implications. We do not provide a review of the literature on the health effects of air pollution, which can be found elsewhere.7,8 Although many air pollution studies have been conducted in the Los Angeles area, the CHS is unique in its focus on chronic effects and its repeated evaluations of prospectively followed cohorts of children. Air quality across the CHS communities is comparable to conditions in other areas of the United States (Table 1
More than 6000 public school children were recruited into the CHS from 12 different communities, which maximized the diversity in air pollution concentrations and mixtures across the region.9 In total, nearly 4000 children in the 4th, 7th, and 10th grades were recruited at the initiation of the study in 1993, and an additional 2000 4th grade schoolchildren were recruited in 1996.2,6,10 At study entry, a questionnaire assessed demographic characteristics of the family and the childs history of asthma, hay fever, and early life respiratory illnesses, as well as outdoor and physical activities, environmental tobacco smoke exposure, housing characteristics, and the familys health history. Diet and genetic characteristics have been evaluated in subsequent years. In addition, yearly questionnaires assess the childrens development of respiratory symptoms and their current activity patterns. Furthermore, lung function has been measured each year via spirometry.11 School absences have been monitored to allow evaluation of the effects of pollution on acute respiratory illnesses.12
As a means of characterizing air quality in each of the 12 study communities, ambient concentrations of O3, PM2.5 (particulate matter less than 2.5 microns in diameter), PM10, NO2, and acid vapors have been measured at central monitoring stations (Table 1
In addition to the crosssectional findings published in 1999,2,6 the ongoing CHS project has yielded a wealth of data from the cohort follow-up, with a major focus on the chronic effects of air pollution. Chronic effects not previously reported were observed with respect to lung function growth and asthma, and short-term effects were observed with respect to school absences (Table 2
Lung function growth was approximately 10% slower among children living in communities with higher NO2 levels and other traffic-related pollutants, including nitric acid vapor and particulate matter.15 This result was replicated in the second cohort of 4th-grade schoolchildren enrolled in 1996,10 and the effect was observed among both normal and asthmatic children. These findings are consistent with longitudinal and crosssectional findings of other investigations.16,17 An improvement was seen in lung function growth rates among children who moved away from the more polluted communities to areas of lower PM10 concentrations, and growth rate retardation was observed among those moving to areas with higher concentrations.18 School absence rates increased with daily fluctuations in O3 levels, particularly when levels rose in communities with low concentrations of PM10 and NO2.12 A modest increase of 20 parts per billion in 8-hour average ozone was associated with an 83% increase in school absences resulting from acute respiratory illnesses. Children with asthma experienced more bronchitis and persistent phlegm production if they lived in communities with more NO2 or particulate pollution.19 This finding accords with results from the Harvard Six Cities Study.20 Given the fact that people with asthma have more bouts of bronchitis than those without asthma, even a modest increased risk in bronchitis rates due to air pollution may result in a considerable burden in terms of increased asthma symptoms in children.13 Children who played team sports and spent more time outside in communities with high ozone levels had a higher incidence of newly diagnosed asthma.21 In communities with low ozone levels, playing team sports was not associated with an increased risk of asthma. Because exercising children exhibit increased rates of ventilation, playing team sports increases doses of ozone and other lung pollutants. This finding is noteworthy, because it was previously believed that air pollution exacerbated asthma among children who already have the disease rather than causing new-onset asthma. A recent Dutch cohort study of newborn children also revealed increased asthma incidence rates among children living in more polluted communities.22
Ongoing components of the CHS aim to determine whether deficits in lung function growth from air pollution in childhood result in diminished maximum attained lung function (which occurs in early adulthood) and to evaluate factors, such as asthma, that may modify the effect of air pollution on attained lung function. For example, children reporting recent respiratory illnesses exhibited measurable and significant decrements in pulmonary function, decrements that were most marked in the small airways.23 By following the cohorts into adult life and repeatedly measuring lung function, it should be possible to distinguish the main effects of acute and cumulative exposures.
Limitations of the CHS are discussed in the articles listed in Table 2 The association between ozone exposures among children playing team sports and new-onset asthma requires further study. Because asthma prevalence rates vary widely between communities for reasons that are not well understood,28 examining within-community variability in air pollution may be an important strategy for clarifying the effects of air pollution on asthma. Preliminary results from the CHS suggest that residential proximity to traffic is associated with asthma prevalence rates.29 In 2002, the CHS began recruitment of a new cohort of 6000 children aged 5 to 7 years, and this cohort provides an opportunity to evaluate the laboratory observation that co-exposure to ozone or to particulate matter in diesel exhaust enhances the effect of allergens in producing asthma and allergies in animal models.30,31 Improved techniques for modeling lung function, developed for the CHS, have demonstrated reduced lung function in asthmatic children, even before diagnosis,32 and these methods are now being applied in an examination of the joint effects of air pollution and asthma on lung function and lung function growth at different ages (K. Berhane, D. O. Stram, W. J. Gauderman, and D. C. Thomas, unpublished data, 2003). The evidence emerging from the CHS supports the hypothesis that genetics and diet are important for respiratory health, and the hypothesis that they may modify the effect of oxidant pollutants is under active investigation.33,34 The observed interaction in the CHS between in utero tobacco smoke exposure and asthma prevalence and lung function is a model for similar interactions that might occur with air pollution.35,36 The effect of in utero tobacco smoke exposure on asthma risk was observed primarily in children with a null genotype for glutathione S-transferase M1; (the null genotype results in a lack of this antioxidant enzyme).37 Observed protective relationships of lung function with dietary magnesium and potassium38 and with vitamin C39 suggest potential avenues for primary prevention.40
The development of good public health policy is based on evaluating overall scientific evidence7 rather than relying on findings from a single study. However, the effects of air pollution on health observed in the CHS provide an example of evidence that improvements in air quality would lessen both acute and chronic respiratory illnesses among children. According to the CHS results, the successful reductions in ozone levels in Southern California have prevented more than 2.8 million school absences involving an economic cost of more than $220 million.41,42 The observation that lung function increased in CHS children who moved to cleaner communities (and decreased in children who moved to more polluted communities)18 strongly suggests that chronic lung function effects are caused by air pollution. Thus, both better compliance with existing standards and further improvements in air quality are needed to protect childrens health.
We distinguish 2 approaches to reducing exposure to air pollution. "Primary strategies" that reduce ambient concentrations of air pollutants must be the main focus of regulatory action, and "secondary strategies" that reduce childrens exposure to air pollution without improving ambient air quality may have a complementary and temporary role (Table 3
Ambient air quality standards for major air pollutants are set to protect public health, and vigorous enforcement of compliance with these standards is a principal regulatory tool in the United States. The standards themselves have been based largely on acute effect studies. The California Environmental Protection Agency, for example, estimates that 400 000 episodes of upper and lower respiratory symptoms in children could be prevented each year in California alone if the new PM2.5 standard of 12 µg/m3 (annual mean) were met.13 Results from the CHS and other recent studies suggest that long-term effects have been underestimated and that the benefits of meeting current standards would be even larger than the states estimates.13,45,46
Compelling evidence from the CHS that lung function is impaired by air pollution is directly relevant to the current debate over the regulation of particulate pollutants. In addition, the emerging evidence that air pollution is a factor in the development of asthma is relevant to the new federal ozone standards under consideration. Nearly 70 million Americans live in areas that exceed existing ozone standards, nearly 10 million live in areas exceeding NO2 standards, and more than 20 million live in areas exceeding standards set for PM10.4 Clearly, complying with current air quality standards would benefit childrens health, and the new evidence strongly endorses the strategy of the California Environmental Protection Agency, which recently set stricter standards (Table 1
Examples of interventions that would reduce pollution and help achieve compliance with air quality standards are presented in Table 3 There is an urgent need for incentives that lead to faster implementation of the "best available technology." However, this goal is hampered by stalled or failed regulatory policy. Delays due to prolonged legal challenges to new air quality standards, long phase-in periods for cleaner diesel engines, and exemptions and delays in holding sport utility vehicles and other larger vehicles (e.g., trucks, ships, school buses) to the same standards as smaller cars create disincentives in regard to the overall reduction of air pollution. No single policy tool is likely to be sufficient to achieve marked reductions in air pollution. A long-term, integrated set of policies to rebuild communities to make them less dependent on fossil fuels for transportation would yield benefits that go far beyond improved health. For example, policies that promote the rapid development and implementation of very low or zero-emission vehicles, combined with strong incentives such as emission-related taxes, road tolls, and fuel prices that would cover all direct and indirect costs of traffic (including costs related to health damage), could strongly influence consumer choice.52,53 Such a strategy would improve childrens respiratory health, mitigate the long-term threats posed by greenhouse gas emissions from mobile sources, and reduce the current heavy dependence on foreign oil.8,5456 Prioritizing policies that lead to zero emission vehicle fleets would also avoid the trade-offs between health and the environment inherent in the promotion of diesel automobiles as a solution to the problem of greenhouse gas production.57 In fact, diesel cars are associated with very little savings of energy or reduction in carbon dioxide levels,53 and they are associated with much higher emission levels of unhealthy particulates. The World Health Organization58 has also proposed integrated regulatory approaches. For example, programs promoting bicycling and walking as transportation options for children59,60 could (1) decrease automobile emissions; (2) reduce the time that children spend in cars, where rates of exposure to certain pollutants and toxic compounds are up to 10 times higher than outdoors61; and (3) promote healthy physical activity in the current generation of increasingly sedentary and obese children.62
Even with the most aggressive efforts to reduce emissions, the current generation of children in the Los Angeles metropolitan area will suffer adverse health effects from air pollution. Thus, policies designed to reduce childrens exposure to air pollution should be considered. Examples that merit further discussion include the following:
In the long term, secondary reduction strategies are limited and have the potential to increase other public health risks. For example, limiting exercise on high pollution days to reduce doses of pollutants entering the lungs may increase the risk of diseases associated with childrens increasingly sedentary lifestyles.62 Walking to school, rather than driving with a parent, may increase childrens exposure unless walking routes and traffic patterns around schools are taken into account.66,67 Air-conditioning in schools would increase energy consumption and emissions from power plants. Furthermore, air-conditioning may contribute to other health problems, such as sick building syndrome.68 Although promotion of dietary antioxidant supplements such as vitamin C or E may be a promising intervention, there is some evidence that vitamin C may act as a pro-oxidant,69 and further evaluation of such an intervention is required before programs could be implemented. Finally, peoples individual decisions to move to more distant, seemingly less polluted suburban areas may result in overall increased levels of emissions if commuting time increases.70 In the long term, secondary strategies will fail to protect the publics health unless they are complementary to emission reduction strategies.8,13,52
The CHS and other studies contribute to the strong evidence that air pollution at levels permitted by current standards is harming childrens health. In addition, on the basis of emerging evidence of chronic effects, risk assessments used in setting regulatory policy most likely underestimate the harm done by currently permissible levels. Our children deserve a visionary public health regulatory policy that addresses these challenges and protects them from sources of air pollution. A policy framework designed to protect children should focus on reducing emissions in the short term. Long-term policies must accomplish a decisive move toward low- to zero-emission vehicles with high fuel economy ratings.
This research was supported by the California Air Resources Board (contract 94-331), the National Institute of Environmental Health Sciences (grants 1P01 ESO9581-04, 1P01 ES11627-01, and 5P30 ES07048-07), the Environmental Protection Agency (grant R 826708-01-0), and the Hastings Foundation.
Contributors N. Künzli led the writing of the article. R. McConnell provided significant writing and technical contributions. D. Bates developed many of the foundations for the article and commented on all versions. T. Bastain contributed to research and to editing. A. Hricko provided policy implications and suggestions and contributed to editing and research. F. Lurmann and E. Avol provided technical expertise and suggestions related to exposure assessments. F. Gilliland provided technical expertise and suggestions regarding genetic epidemiology. J. Peters made significant contributions to writing and editing. Accepted for publication April 18, 2003.
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