Traffic- Related Air Pollution: A Critical Review of the Literature on Emissions, Exposure, and Health Effects

1. Traffic- Related Air Pollution:A Critical Review of the Literature on Emissions, Exposure, and Health Effects Society for Risk Analysis November 19, 2009 Maria Costantini Health Effects Institute

2. Goals of the Review Summarize and synthesize relevant information on air pollution from traffic and its health effects linking • Information on tailpipe emissions with human exposure to traffic –related pollution • Human exposure to traffic pollution with human health effects (epidemiology) • Epidemiologic associations with toxicological results A preprint of the report released in May 2009 Formal Report published in January 2010

3. HEI Traffic Review Panel Kenneth Demerjian—SUNY, Albany Mark Frampton—U Rochester Michael Jerrett—UCBerkeley Frank Kelly—King’s College Lester Kobzik—Harvard SPH Nino Künzli—IMdM, Barcelona Brian Leaderer—Yale SPH Thomas Lumley—U of Washington SPH Frederick Lurmann—Sonoma Tech. Inc Sylvia Richardson—Imperial College Jon Samet—Johns Hopkins Ira Tager—UCBerkeley, Chair Michael Walsh—Consultant

4. Significant progress has been made in reducing pollutant emissions from motor vehicles despite increases in number of vehicles and vehicle miles traveled Increased urbanization and urban populations and changes in land use have: Increased dependence on motor vehicles and traffic congestion Emissions from Motor VehiclesThe Current Context more people are near traffic sources of pollution

5. Emissions from Motor Vehicles Emissions data and emission inventories are needed to: • Understand the relative contribution of motor vehicles emissions to air pollution in total and at specific locations • Contribution to PM, CO, NOx,, VOCs • Describe exposure • Trends in emissions in the context of transportation plans and introduction of new control technologies and new fuels • Improve the quality and range of pollutant surrogates

6. Pollutant Surrogate Traffic Pollution • CO • NO2 • PM2.5 • EC (also referred to as BC, BS, or soot) • Ultrafine PM • Benzene

7. Size Distribution of PM 3 main classes of PM Coarse - PM2.5-10 mass Fine - PM2.5 mass Ultrafine – PM0.1 number Courtesy of David Kittelson and Winn Watts, 2009

8. Gradients of NO2 and PM from Source From Beckerman et al 2008

9. CO EC NO2 UFPM Road to 100-400 m Road to 200-500 m Road to 100-300 m Spatial Extent Estimates

10. Assessment of Exposure to Primary Traffic-Generated Air Pollution Surrogates of traffic exposure used in epidemiologic studies • Pollutant surrogates (e.g., NO2, PM, EC/BS, CO, benzene, etc.) • Traffic exposure models • Estimate of traffic density or intensity • Distance from and/or length of roadways • Complex models that provide surrogate concentrations • Geostatistical interpolation, dispersion, land-use, and hybrid model Direct measures of traffic

11. Conclusions on Traffic Exposure Surrogates • None of the pollutant surrogates considered met all criteria for an ideal surrogate • CO, benzene, and NOx [NO2] found in on-road vehicle emissions are components of emissions from all sources and are also contributed by indoor sources. They have substantial variability across locations. Can be useful if measured with final spatial resolution. • PM2.5 as a surrogate of traffic pollution is of limited value because it is emitted by many sources and is well mixed within a region • UFPM have not been used in epidemiologic studies so far because the characterization of their spatial concentration gradients pose a significant challenge

12. Conclusions on Traffic Exposure Surrogates (cont.) • Exposure models have various degrees of utility to health studies depending on the quality of the input data • The measure of distance to road is the most error-prone and the least specific • Measures of traffic density and traffic flow are more specific • The hybrid model provides a feasible “best” estimate of exposure • Combines a model with time-activity data or personal monitoring

13. Epidemiology

14. Epidemiology Criteria for Inclusion of Studies Based on type of exposure metric • Only studies in which the pollutant surrogates of exposure used were documented to have derived primarily from traffic or were measured in proximity of the residences and the roadways • Studies based direct measures or models of traffic Exposure based on traffic density or derived from exposure models (other than proximity) considered to be “best” surrogates”

15. Epidemiology Criteria for Causal Inference 4 categories1 used to infer causal association based on how well studies controlled for confounding, on the consistency of the findings across studies, and on the quality of the method to estimate exposure to primary traffic-generated pollutants • Sufficient evidence- all studies were of appropriate quality and at least one study measured traffic density or used modeled exposure • Suggestive but not sufficientevidence– as A, but studies only used distance measures • Inadequate and insufficient evidence • Suggestive of no association 1Adapted from US Surgeon General on the health consequences of ETS

16. Epidemiology Health Outcomes Evaluated • Mortality (all cause, cardiopulmonary) • Cardiovascular morbidity • Respiratory outcomes (children and adults) • Asthma—childhood/adult • Respiratory symptoms • Health care utilization for respiratory problems • Lung function • COPD • Non-asthmatic allergy (children) • Birth outcomes • Cancer (children and adults)

17. Long-Term Traffic Exposure and Cardiopulmonary Mortality Synthesis of Evidence “Suggestive but insufficient” to infer causal association Reasons Too few studies Relative imprecision of most estimates

18. Traffic Exposure and Asthma Incidence (in Children) Synthesis of Evidence “Sufficient” OR “suggestive but insufficient” to infer causal association Reasons Studies including both traffic-specific pollutants and density measures most consistent Studies on incidence were consistent with studies of prevalence

19. Exacerbation of Asthma Symptoms Increase in Wheeze in Children

20. Exacerbation of Asthma SymptomsIncrease in Wheeze in Children (cont.) Synthesis of Evidence Exacerbations with asthma—”Sufficient” to infer causal association Reasons Large number of studies with adequate control for confounding and mostly precise effect estimates

21. Other Respiratory Symptoms(in Children)

22. Traffic Exposure and Allergies(in Children) Synthesis of evidence “Inadequate and insufficient” to infer a causal association Reason With a few inconsistent exceptions, results based on the skin-prick test or allergen-specific IgE failed to show associations with any of the traffic-pollution Results for other endpoints (such as hay fever, eczema, itchy rash) were inconsistent

23. Traffic Exposure and Allergies(in Children)

24. Conclusions

25. Exposure – Area of Impact • Traffic-related pollutants impact ambient air quality on a broad spatial scale ranging from roadside, to urban, to regional background • Based on synthesis of evidence, 300-500 meters from a major road was identified as the near-source area most impacted by traffic; variations exist depending on meteorology, background pollution, and local factors

26. Conclusions From Epidemiologic Studies • “Inadequate and insufficient” evidence to Infer causal associations • Adult onset asthma • Health care utilization for childhood and adult respiratory diseases • COPD • Non-asthmatic allergy • Birth outcomes • Cancers • “Sufficient ” evidence to Infer causal associations • Exacerbation of asthma • Asthma incidence in children • “Suggestive but insufficient” evidence • Mortality (all-cause and cardiovascular) • Cardiovascular morbidity • Decreases in lung function • General respiratory symptoms

27. Comparison of Epi and Tox Conclusions Cardiovascular morbidity Epi: Suggestive, but not sufficientTox: Evidence from tox not sufficient in isolation, but consistent with some epi findings. A case could be made for a potential causal role of traffic pollutants in cardiovascular-disease morbidity Exacerbation of asthma Epi: Sufficient Tox: Evidence supportive of epi conclusions, but studies are limited in the endpoints evaluated Non-asthmatic allergy Epi: Inadequate and insufficientTox: Data supported a stronger inference that the epi (by providing mechanistic evidence for associations of traffic pollution and IgE-mediated allergic reactions), but studies used non relevant exposure routes and doses Birth outcomes Epi: Inadequate and insufficient No overlap in outcomes between epi and tox; synthesis is not possible Cancers Epi: Inadequate and insufficient Evidence from in vitro and long-term studies to DE for DNA damage and carcinogenicity, but it is difficult to relate results to humans; synthesis is premature

28. For a version of the report go to www.healtheffects.org