# Presentation: 445752

## Transportation Perspectives on Adverse Health Impacts of Air Toxics

**Dr. Aviva Brecher **
**and**
**Nicole Rossbach**
***TRB 466, Jan 14, 2003:**** *
***“******AIR TOXICS: THE NEXT POISON PILL FOR TRANSPORTATION?”***

## TRANSPORTATION SYSTEM PERSPECTIVE

**MULTIMODAL FLEET: **
**~200 M CARS, 220 M BUSES AND TRUCKS,  100 K TRANSIT (LIGHT, HEAVY RAIL, TROLLEYS, BUSES), ~10K COMMERCIAL JETS, 200K GAA, 20.5K RAIL LOCOMOTIVES, 12.8K WATERCRAFT**
**BTS 2002 TRANSPORTATION INDICATORS:**
**HWY: 114,505 mi NHS ROADS; 3.951 Bmi OTHER ROADS**
**URBAN TRANSIT (ROUTE-mi): 158 Kmi BUS, TROLLEY; 7.3 Kmi RAIL TRANSIT (COMMUTER, LIGHT, HEAVY)**
**RAIL, TRACK-mi: 22.7 Kmi AMTRAK, 171 Kmi FREIGHT**
**ALSO: AIR, MARINE AND PIPELINES (OIL AND GAS T&D)**
**BALANCING TEA-21 AND TEA-3 SURFACE TRANSPORTATION OBJECTIVES :**
**Economic, mobility and access, security, benefits vs.**
**Costs and risks of adverse transportation energy,  environmental and health effects**

## COMPARATIVE RISK PERSPECTIVE-1

**Regulatory thresholds (1 in a million) and value of life in RIA differ widely across agencies - harmonize**
**Acceptability threshold: voluntary vs. involuntary risk**
**Lifetime cancer probability: 1 in 2-men; 1 in 3-women**
**Lifetime risk of dying from cancers:  1 in 7 (annual 1/550)**
**US mortality rate decreased  18% in last 20 yrs, 23% of ’98 deaths due to cancer, down by 6% from ‘78**
**Days of Life Expectancy lost by: **
**smoking 1 pack/day- 2200 d; **
**overeating (200 cal/d) - 400 d; **
**riding in cars- 200 d; drowning- 40 d; **
**air pollution (est., all sources)- 25 d **

## COMPARATIVE RISK PERSPECTIVE-2

**“**_**Risk-A Practical Guide**_**...” ****(2002, Ropeik and Gray, Directors, Harvard Center for Risk Analysis)**
**Risk= probability (P) x consequence (C)**
**Risk Meter:  rank P and C on scale of 0-10**
**Motor Vehicle Crashes:  8-9 for P, 5-6 for C **
**Air Pollution:  **
**Particulates: 6-7 for P and for C (many people exposed with  sometimes severe conseqs.)**
**Smog: 2-4 for P, 1-3 for C (sporadic, temporary and localized exposure episodes, association with asthma and premature mortality of sensitive individuals)**
**Air Toxics: 1 for P, 1 for C (exposure levels are so low that they are unlikely to be very hazardous to more than very few, sensitive people)**
**Indoor Air Quality:  4-6 for P, 2-4 for C**

## R&D PROJECT ON PUBLIC HEALTH IMPACTS OF MOBILE SOURCE AIR TOXICS (MSAT)

**FHWA AQ team through Volpe Center**** **
**1 of  5 complementary projects**
**KEY OBJECTIVES: **
**Critical review and synthesis of research and current literature on health effects of air toxics from surface transportation sources (including fine particulates, synergistic effects of exposure to  multiple air pollutants)**
**Improved understanding of state of knowledge on human  health effects, uncertainties (data gaps, analysis, modeling, projections) **
**Inform strategies to reduce MSAT emissions, initiatives, standards, policies and R&D programs for TEA-3 reauthorization**

## CHAIN FROM POLLUTANTS EMISSIONS INVENTORY TO INFERRED ADVERSE HUMAN HEALTH IMPACTS 

**Adverse Health  Effects**
**(cancer, non-cancer;direct/indirect; cells, animals, epidemiol. dose-response, risk ranking)**

**Population Exposure**
**(env., occup’l.,**
**sensitive subgroups) **

**Model & Measure**
**Emissions**
**(chem. species, amounts)**

**Transportation Sources**
**(fleet profile, modal shares, VMT, emission factors,controls)**

## ‘99 NAAQS EMISSIONS BY SOURCE 

**‘****99** **NAAQS EMISSIONS BY SOURCE**** **

- Table 1.  Criteria pollutant and corresponding percent source contribution (Source: EPA 1999b, *EPA 2002b).

## VOLATILE ORGANIC COMPOUNDS (VOC) BY SOURCE

- Figure 1.  Percent source contribution of volatile organic compounds.

## EPA PROJECTS: VMT WILL DOUBLE, VOC (HAP) WILL HALVE

- Figure 2.  Depiction of predicted steadily increasing vehicle miles traveled while VOC and NOx emissions decrease.

##  MODAL SHARES OF TRANSPORTATION EMISSIONS

** ****MODAL SHARES OF TRANSPORTATION EMISSIONS**

- Figure 3.  Depiction of transportation modal shares of specific PM10, VOC, NOx, and CO.

## POTENTIAL HEALTH EFFECTS OF CRITERIA POLLUTANTS 

**POTENTIAL HEALTH EFFECTS** **OF ****CRITERIA POLLUTANTS**** **

- Table 2.  Description and list of potential health effects of criteria pollutants.

## 33 URBAN AIR TOXICS (UATs)

**Acetaldehyde**
**Acrolein**
**Acrylonitrile**
**Arsenic Compounds**
**Benzene**
**Beryllium Compounds**
**1,3-Butadiene**
**Cadmium Compounds**
**Carbon Tetrachloride**
**Chloroform**
**Chromium Compounds**
**Coke oven emissions**
**Dioxin/Furans**
**1,3-Dichloropropene**
**Ethylene dibromide**
**Ethylene dichloride**
**Ethylene oxide**

**Formaldehyde**
**Hexachlorobenzene**
**Hydrazine**
**Lead Compounds**
**Manganese Compounds**
**Mercury Compounds**
**Methylene Chloride**
**Nickel Compounds**
**Perchloroethylene**
**Polychlorinated**
**biphenyls (PCBs)**
**Polycyclic organic matter, POM**
**(sum of  7 polycyclic aromatic hydrocarbons)**
**Propylene Dichloride**
**Quinoline**
**1,1,2,2-tetrachloro-ethane**
**Trichloroethylene**
**Vinyl chloride**
** **

## HAP CONTRIBUTIONS BY SOURCE

- Figure 4.  Source contribution of HAP.

- Figure 5.  Source contributions of air toxics.

## EPA’S MOBILE SOURCE AIR TOXICS (MSATs)

**Acetaldehyde**
**Acrolein**
**Arsenic compounds**
**Benzene**
**1,3-Butadiene**
**Chromium Compounds**
**Dioxin/Furans**
**Diesel Exhaust-41 toxics**
**Ethylbenzene**
**Formaldehyde**
**n-Hexane**

**Lead Compounds**
**Manganese Compounds**
**Mercury Compounds**
**MTBE**
**Naphthalene**
**Nickel Compounds**
**POM (7 PAHs)**
**Styrene**
**Toluene**
**Xylene**

- Diesel exhaust contains 41 toxic compounds (CARB)

## AMOUNTS OF MSATs

- Table 3.  1990 national emission estimates for urban HAP emitted from mobile sources  (EPA 2000, National Air Toxics Program:  The Integrated Urban Strategy, Report to Congress).

## HEALTH EFFECTS OF 3 MSAT’s 

**HEALTH EFFECTS OF 3 MSAT’s**

- Table 4.  Carcinogenic and non-carcinogenic effects associated with exposure to benzene, 1,3-butadiene, and formaldehyde.

## CARCINOGENICITY CLASSIFICATIONS FOR 5 MSAT’s

**CARCINOGENICITY CLASSIFICATIONS FOR 5 MSAT’s**

- Table 5.  Different classification schemes and rankings for 5 MSAT’s.

## NATA HEALTH EFFECTS

_**ASSESSMENT LIMITATIONS**_**:**
**Data, location, time, sources, model assumptions, health end effects, risk inferences; ****Confounders**
_**VARIABILITIES**_**: **
-  **Emissions, air concentrations, exposures and risks **
_**UNCERTAINTIES**_**:**
**Measuring dose; Multiple pollutants and simultaneous exposures; Acute vs. chronic exposures; Specificity of evidence (animal models); Dose-response; Thresholds or functions; Epidemiology evidence (all are exposed) **

## NATA UNCERTAINTIES

_**MODELING**_**:  **Modeling default assumptions in NATA 93, 96, 99 Transportation Emissions estimates (MOBTOX5b) based on emissions factors by inventory groups; fleet and fuel profile; driving cycle, VMT; 99 NATA not published; HAPEM-Hazardous Air Pollutant Exposure Model
_**DATA QUALITY**_**:  **Sparse, non-uniform coverage by monitoring stations (in space and time, speciation, source/type attribution); States are collecting, reporting, analyzing NATA data
_**INTERPRETATION:**_**  **Conservatism, margin of safety

## EXAMPLE: PARTICULATES HEALTH EFFECTS (DPM IS A TAC)

**NATIONAL MORBIDITY, MORTALITY& AIR POLLUTION STUDY (NMMAPS) **
**Documented association of increased risk with PM exposure in 90 US cities (22- time series, 2- chronic exposure studies)**
**LINEAR NO THRESHOLD (LNT), ACUTE RESPIRATORY AND CARDIO-VASCULAR EFFECTS: **
**Increased bronchitis and asthma, depressed lung function, arrythmia... but PM alone, + co-pollutants?**
**TEMPORAL AND SPATIAL VARIABILITY OF PM VS HEALTH EFFECTS: **
**Urban hi traffic density and highways are PM “hotspots” (socioeconomic confounders); Local, regional, global ave.?**
**VULNERABLE SEGMENTS**** **
**Children, pregnant women, elderly, those with chronic respiratory or heart disease and lower immune system function**

## STATE OF SCIENCE ON  PM HEALTH EFFECTS 

**MORTALITY RATE INCREASE: **
**PM10: .5% - 1% for each 10 ug/m3 increase, NMMAPS now revised down to .2 %; PM2.5: 1.6% per 10ug/m3 **
**CANCER RISK RATIO (RR): **
**RR**  **for lung cancer w.  sulfates and particulates were 1.36 and 1.03, respectively; unclear which constituents cause it.**
**HEI DIESEL EMISSIONS AND LUNG CANCER STUDY (99):  **
**RR  .7 to 1.3.; diesel engines contribute mostly PM2.5  **
**NON-CANCER RISKS: **
**Cardiopulmonary disease (1.26 and 1.31 RR for sulfates at 19.9 ug/3, particulates at 24 ug/m3) **
**Respiratory disease (.8% to 1% increase per 10ug/m3 increase in PM10) **
**Asthma (1.9% increase per 10 ug/m3 increase in PM10)**

**Notes:**
Pope, C.A. III, et al.  1995.  Particulate Air Pollution as a Predictor of Mortality in a Prospective Study of U.S. Adults.  American Journal of Respiratory Critical Care Med.  Vol. 151: 669-674.  
This landmark study followed a prospective cohort initiated in 1980 to evaluate the effects of particulate air pollution on mortality.  They studied data, based from the American Cancer Society Cancer Prevention Study II, from 151 U.S. metropolitan areas in 552,138 adults.  They found that particulate air pollution was associated with cardiopulmonary and lung cancer mortality but not with mortality due to other causes.  Additionally, mortality risk ratios indicated that lung cancer is more strongly associated with sulfate particles than fine particulate mass in general.  Finally, the study asserted that these associations were not due to confounding, particularly smoking.  

## HEI NMMAPS PM-10 AND CO-POLLUTANTS HEALTH EFFECTS IN 90 LARGEST US CITIES

**Figure 6.  NMMAPS Analyses of PM vs. Other Pollutants -mean effect estimate revised from .41% ****	****increase in mortality for every 10 micrograms increase in PM10 to .21%  (HEI 2002). **

**HEI NMMAPS PM-10 AND CO-POLLUTANTS HEALTH EFFECTS IN 90 LARGEST US CITIES**

## RESEARCH NEEDS FOR PM HEALTH EFFECTS

**PM MASS (CURRENT NAAQS) OR NUMBER, SIZE DISTRIBUTION VS HEALTH IMPACTS (CARDIO-VASCULAR, RESPIRATORY? OTHER?) **
**MONITORING AND AVERAGING: **
**Equipment, sampling frequency, averaging, locations, duration, variability, sources, “hotspots” **
**PARTICLE CHARACTERIZATION:**
**Size, surface area, composition vs. nocivity, recovery mechanisms  **
**SPECIATION: **
**Soot, co-pollutants (SO2, O3, CO), sulfates (in NE), nitrates (in W. US), acids, reactive transition metals, biogenic allergens**
**BIO-MARKERS AND BIO-EFFECTS FOR PM FRACTIONS**
**TOXICOLOGY AND EPIDEMIOLOGY: **
**Time series vs long-term, retrospective vs prospective, acute vs chronic, controlled exposures, mechanisms, dose-response (LNT vs thresholds), reversible vs permanent damage****?**

## STATUS OF HAP HEALTH EFFECTS

**EXPERTS FROM HARVARD SCHOOL OF PUBLIC HEALTH, HEI: HAP HEALTH RISKS APPEAR SUBSTANTIALLY LOWER THAN FOR PM, OZONE**
**MULTIPLE AIR TOXICS EMISSIONS STUDIES (MATES I AND II): **
**Best data (12 yrs), no direct DPM measurement (C as surrogate)**
**Risk of cancer has decreased by x4-5 (’86-’98)**
**10 key risk drivers (DPM, benzene, 1,3 butadiene, formaldehyde) **
**50% of toxicity-weighted emissions from on-road **
**Urban “microenvironments,” highways are “hotspots” for PM and HAP**
**Elevated cancer risk in urban “hotspots” **
**Upgrade monitoring, inventories, models, health risk estimates**
** **

## MULTIPLE INITIATIVES UNDERWAY WILL REDUCE HAPs

**MACT AND NATIONAL EMISSIONS STDS (NESHAP) **
**EPA’s stationary (major, area) sources**
**LARGE REDUCTIONS IN HAPS PROJECTED BY 2020, NO SPECIFIC CAPS ON MSAT PER SEC 202(L), 2001**
**LINKAGE OF HAP AND NATA TO NAAQS IN NEI**
**2004- 2007 PHASE-IN OF NEW REGS **
**Diesel vehicle-fuel system, Tier 2, caps on Heavy-Med engines, diesel locomotives, marine and off-road sources, school buses, Integrated Urban Air Toxics Strategy (UATS)**
**EPA’S REVISED “NEW SOURCE REVIEW” **
**relaxed controls**
**stretched timetable for fixed source HAP emissions will constrain  mobile sources**

## PROGRESS, PROGNOSIS  FOR HAP CONTROL & HEALTH EFFECTS 

**EPA’s Natl. Emissions Inventory (NEI), Integrated Urban Toxics Strategy (’99), and Implementation Report (2000) for HAPs**
**40 CFR  80, 86 – Control of Emissions Mobile Sources HAPs, Final Rule, 3/20/01: will cut MSATs:** **benzene, formaldehyde, 1,3-butadiene, and acetaldehyde 67 to 76 %;  DPM- 90% by 2020**
**Updates of EPA’s Health Effects Notebook, NATA, Integrated Risk Information System (IRIS)**

**Address data gaps, model default assumptions, errors, uncertainties, EJ (hotspots)**
**Identify and prioritize HAP by environmental health risks**
**Focus on health  risk prevention, mitigation “worst-first”**
**Relaxing major source NSR  increases pressure on mobile sources controls**
**“****Dieselization” to improve CAFE and GHG may increase particulates, HAP & smog health hazards**
**NAAQS non-attainment, NEPA and transportation conformity**

## MSAT  STATUS AND FORECAST

**EMISSIONS REDUCTIONS TO 2020:**
**Synergy of regulatory caps on all source types, new vehicle emissions controls and clean fuels technologies, state and regional clean vehicles and green cities, community and grassroots transportation and health initiatives.**
**Energy efficiency and air quality goals must be balanced**
**Vehicle specific regs may not be needed, but evaluate control technologies potential for HAP reductions **
**NEED TO COORDINATE R&D: **
**Improve models and data for emissions inventories by source, understand exposures, risk and environmental health effects**
**Meet AQ challenges of Healthy People 2010 public health goals**
**Active collaboration with federal, state environment and health agencies; nonprofits (HEI), NAS and universities **

## KEY ISSUES FOR MSAT CONTROL, MITIGATION

**NO NEED FOR SEPARATE MSAT REGULATIONS **
**HAPS are part of  PM and VOC (as O3 precursor) controlled emissions**
**Enforcing ‘97 NAAQS and phase-in of new regs (HDE, diesel, non-road) will reduce HAPS substantially, thus health risk**
**RISK-BASED PRIORITIZATION:**** **
**EPA prioritizes HAP reduction by toxicity, not amounts, yet caps mass**
**NO NATIONAL HAP MONITORING SYSTEM NOW**
**Standardize, improve monitoring coverage to resolve, assess HAP trends by site, sources**
**SIMILAR HEALTH EFFECTS FOR NAAQS, HAP**** **
**How to “unbundle” and apportion  health risk?**
**SUPPORT EPA’S 13 RESEARCH NEEDS FOR UATs IN  EXPOSURE ASST., HEALTH EFFECTS, DOSE-RESPONSE, RA/RM- TO INFORM SENSIBLE MSAT REGS.**

## FINAL CAVEATS

***Environmental Health Risk Assessment is  a very complex  process, under active research***
***Many interpretations are possible for same dataset, need interagency consensus***
***Need cells, animals HAP-specific mechanistic models for cancer, non-cancer (NTP protocol)***
***220 cancers, as >2-step process (initiation, promotion, co-promotion) with long incubation times***
***Epidemiological association is NOT  proof of causality; Absence of Evidence is NOT Evidence of Absence***