Health and Environmental Assessment

of the Use of Ethanol as a Fuel Oxygenate

UCRL-AR-135949 Vol. 5

Report to the 

California Environmental 

Policy Council 

in Response to 

Executive Order 

D-5-99

VOLUME

Potential 

5

Health Risks 

of Ethanol 

in Gasoline 

December 1999
Potential Health Risks of

Ethanol in Gasoline

Office of Environmental Health Hazard Assessment

California Environmental Protection Agency

December 1999
i

Table of Contents

1. Introduction...............................................................................................................................1

1.1. Objective ............................................................................................................................1

2. Hazard Identification: Chemicals of Concern.............................................................................2

3. Dose-Response Assessment........................................................................................................2

3.1. Values for Assessing Potential Health Impacts from Inhalation Exposures......................3

3.1.1. Carcinogenic Endpoints............................................................................................3

3.1.2. Noncancer Endpoints................................................................................................3

3.1.2.1. Acute, One-Hour Inhalation Exposures...........................................................3

3.1.2.2. Annual Average Inhalation Exposure Concentrations.....................................4

3.2. Values for Assessing Potential Health Impacts from Exposure via Drinking

Water.................................................................................................................................6

3.2.1. Public Health Goals (PHGs).....................................................................................6

4. Exposure Assessment: Sources of Exposure Data.....................................................................7

5. Methodology Used for Quantifying Cancer and Noncancer Risks .........................................12

5.1. Estimating Cancer Risk....................................................................................................12

5.2. Estimating Noncancer Risk..............................................................................................12

6. Risk Characterization...............................................................................................................14

6.1. Inhalation – Cancer and Noncancer Effects.....................................................................14

6.1.1. Acetaldehyde...........................................................................................................14

6.1.2. Benzene...................................................................................................................15

6.1.3. Butadiene ................................................................................................................15

6.1.4. Ethanol ....................................................................................................................16

6.1.5. Formaldehyde .........................................................................................................16

6.1.6. Methyl t-Butyl Ether (MTBE) ................................................................................17

6.1.7. Peroxyacetyl Nitrate (PAN)....................................................................................18

6.2. Risk Characterization for Other Compounds of Concern: Toluene, Xylenes,

Isobutene, n-Hexane. ......................................................................................................22

6.3. Cumulative Cancer Impact of Multiple Chemical Exposures .........................................23

6.4. Cumulative Noncancer Impact of Multiple Chemical Exposures ...................................25

6.5. Health Impacts of Drinking Water Contamination by Gasoline Components ................28
ii

6.6. Uncertainties and Data Gaps............................................................................................29

6.6.1. Uncertainties in Dose-Response Assessment .........................................................29

6.6.2. Uncertainties in Exposure Assessment ...................................................................30

7. Research Needs.........................................................................................................................32

8. Summary / Conclusions............................................................................................................35

9. References.................................................................................................................................36

Appendix A. Toxicity Summaries ............................................................................................. A-1

Appendix B. Response to Comments.........................................................................................B-1
iii

List of Tables

Table 1. Health Assessment Values and Draft “Health Protective Concentrations”

(HPCs).............................................................................................................................5

Table 2. Health Assessment Values for the Criteria Air Pollutants..............................................6

Table 3. Health Assessment Values and Draft “Health Protective Concentrations” for

Assessing Potential Health Impacts of Ethanol in Gasoline – Oral exposures

from Drinking Water.......................................................................................................6

Table 4, Atmospheric Concentration Estimates: Range of Predicted 1997 and 2003 Air

Quality for the South Coast Air Basina...........................................................................9

Table 5a. Range of Estimated Maximum Noncancer Hazard Quotients (HQ) for Various

Scenarios in the South Coast Air Basin ........................................................................19

Table 5b. Range of Estimated Maximum Noncancer Hazard Quotients (HQ) for Various

Scenarios in the South Coast Air Basin – Criteria Air Pollutants.................................20

Table 5c. Range of Estimated Maximum Lifetime Cancer Risk Values for Various

Scenarios in the South Coast Air Basin ........................................................................21

Table 6. Comparison of Estimated Maximum Pollutant Levels in California (based on

South Coast Air Basin Data for 1996-1997) and Health Assessment Values...............22

Table 7. Lifetime Cancer Risk from Individual Chemicals and Cumulative Lifetime

Cancer Risk for Each of the Five Fuel Scenarios. ........................................................24

Table 8. Maximum Acute Hazard Quotients (HQ) and Cumulative Acute Hazard

Indices (HI) for Eye Irritation for Each of the Five Fuel Scenarios..............................26

Table 9. Maximum Acute Hazard Quotients (HQ) and Cumulative Acute Hazard

Indices (HI) for Respiratory Irritation For Each of the Five Fuel Scenarios................26

Table 10. Maximum Chronic Hazard Quotients (HQ) and Cumulative Chronic Hazard

Indices (HI) for Respiratory Irritation for Each of the Five Fuel Scenarios.................27

Table 11. Research Needs for More Complete Understanding of the Potential Health

Effects of Ethanol in Gasoline. .....................................................................................32

Table 12. Key Issues to be Resolved in Order to Further Our Understanding of the

Potential Health Effects of Ethanol in Gasoline ...........................................................33
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OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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1. Introduction

On March 25, 1999, Governor Gray Davis issued Executive Order D-5-99 which stated that,

while the gasoline additive, methyl tertiary-butyl ether (MTBE), has benefited California by

decreasing air pollution, it also poses an environmental threat to groundwater and drinking water.

Weighing all of the evidence, the Governor declared that there is significant risk to the

environment from using MTBE in gasoline in California. As a result, the Governor assigned

tasks, by way of the Executive Order, to various designated state agencies, regarding the

reformulation of gasoline in the State. Task 10 requires the California Air Resources Board

(CARB) and the State Water Resources Control Board (SWRCB) to conduct an environmental

fate and transport analysis of ethanol in air, surface water, and ground water. It further requires

the Office of Environmental Health Hazard Assessment (OEHHA) to prepare an analysis of the

health risks of ethanol in gasoline, the products of incomplete combustion of ethanol in gasoline,

and any resulting secondary transformation products. This draft report, prepared by OEHHA, is

the analysis of the potential public health impacts of ethanol as an oxygenate in gasoline.

1.1. Objective

The objective of this document is to present an evaluation of the public health impacts of

ethanol as an oxygenate in gasoline. In order to give the analysis a frame of reference, the

potential health impacts of ethanol in gasoline have been evaluated in comparison to the current

MTBE formulation, as well as to gasoline with no oxygenate. This evaluation includes an

analysis of evaporative emissions, tailpipe (exhaust) emissions, as well as atmospheric

transformation products that are produced as a result of the use of ethanol in gasoline. Four

gasoline formulations were selected by CARB for analysis, all formulations fully complying

with existing air pollution regulations. The formulations are as follows:

• Current MTBE-based California Phase 2 Reformulated Gasoline (CaRFG),

• Ethanol-based (with oxygen content of 3.5%),

• Ethanol-based (with oxygen content of 2.0%), and

• A non-oxygenated fully complying fuel.

The CARB model produced estimates of the total concentrations of specific pollutants in

ambient air from all sources (emissions from stationary and mobile sources, and atmospheric

transformation products). Generation of these estimates is described in detail in the report

contributed by CARB: the results are cited here without modification. Rather than evaluating the

health impact of each fuel-related pollutant, this report focuses on the differences in combustion

by-products, evaporative emissions, and atmospheric transformation products that occur from

use of one fuel versus another. It is not intended to assess the overall impact of gasoline usage

regardless of type, or the adequacy of current regulatory controls in limiting the impacts of this

usage on public health.
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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In conducting a quantitative assessment of the relative health impacts of the different fuel

formulations, we used estimates of total air concentrations modeled by CARB, and calculated the

risk levels associated with these concentrations. However, our confidence in these lifetime

cancer risk estimates, and acute and chronic hazard indices, is lower than our confidence in the

relative differences in risk estimate or hazard index associated with the different fuel scenarios.

This arises because of the intrinsic uncertainties in the CARB exposure modeling and the risk

assessment processes.

While this assessment focuses primarily on the potential impacts from emissions into the

ambient air, an evaluation of potential risks from groundwater contamination by fuel components

is also included. This evaluation centers primarily on the differences between MTBE and

ethanol in groundwater.

2. Hazard Identification: Chemicals of Concern

In examining the health risks of ethanol in gasoline, we considered the impacts from

evaporative emissions, exhaust (tailpipe) emissions, as well as secondary transformation

products formed in the atmosphere. Evaporative emissions of unburned gasoline occur primarily

during refueling at the pump, from fuel spills, and directly from carburetors and other fuel

system components of automobiles. Exhaust emissions include unburned fuel and other products

of incomplete combustion. Many of these products, particularly emissions of hydrocarbons and

nitrogen oxides (NOX), together are critical precursors in the formation of ozone and other

atmospheric transformation products.

CARB provided the speciation profiles for the air emissions and modeling to determine

concentrations of key chemicals from the four fuels. OEHHA focused this analysis on key

chemicals associated with fuel use and potential changes in air concentration of those chemicals.

Selection of chemicals of concern initially relied on the identification of representative fuel

constituents and atmospheric contaminants by CARB, and a preliminary assessment of

toxicological data available from secondary sources in the literature. The chemicals determined

to be the most important in terms of public health risks which were selected for more detailed

evaluation in this report are: 1) the oxygenates MTBE, ethanol; 2) Combustion products

1,3-butadiene, formaldehyde, acetaldehyde, carbon monoxide; 3) Evaporative emittents benzene,

hexane, and toluene; and 4) Atmospheric transformation products peroxyacetyl nitrate (PAN)

and ozone. Summaries of the toxicity of each of these compounds are included with this

document as Appendix A.

3. Dose-Response Assessment

In a risk assessment, health impacts are quantified using health assessment values. These

values characterize the dose-response relationship, that is the relationship between exposure to

an agent and the incidence of an adverse health effect in an exposed population. In this risk

analysis, health assessment values used to quantify risks are those currently available from

Cal/EPA and U.S. EPA as described below. In the absence of adopted health assessment values
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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suitable for estimating potential health impacts from the chemicals of concern, OEHHA used

‘proposed’ numbers that have been developed under other California regulatory programs that

are currently undergoing scientific peer review. In cases where ‘proposed’ numbers were not

available, OEHHA calculated ‘health protective concentrations’ for the purpose of this report.

The sources of adopted values and proposed values currently undergoing scientific and public

peer review, as well as the methodology used to calculate draft ‘health protective

concentrations,’ are all described below. The health assessment values used in this report are

shown in Tables 1-3. The derivation of all proposed numbers and draft numbers are included in

the chemical summaries in Appendix A.

3.1. Values for Assessing Potential Health Impacts from

Inhalation Exposures

3.1.1. Carcinogenic Endpoints

Risks from exposure to a carcinogen are quantified using potency values. A carcinogenic

potency is an estimate of the slope of the dose-response curve at low exposure concentrations.

Potency values are expressed in units of inverse dose, either as a cancer potency or slope factor

(i.e., units of (mg/kg-day)-1) or, for inhalation exposures, as a unit risk factor (i.e., units of

(μg/m3

)

-1). These values represent the theoretical probability of extra cancer cases occurring in

an exposed population assuming a 70-year lifetime exposure. Potencies may be derived from

animal or human data, and their derivation takes into account the available information on

pharmacokinetics, mechanism of carcinogenic action, and the effects of different models on low

dose extrapolation. The unit risk or cancer potency factors used in this report are a 95% upper

confidence limit of the slope of the dose-response curve, and thus represent an upper estimate of

the risk.

For this risk assessment, unit risk factors used in inhalation risk calculations are those

currently available from Cal/EPA and U.S. EPA. These values, and information on how they

were derived, are documented in the “Air Toxics Hot Spots Program Risk Assessment

Guidelines, Part II: Technical Support Document for Describing Available Cancer Potency

Factors” (OEHHA, 1999b).

3.1.2. Noncancer Endpoints

3.1.2.1. Acute, One-Hour Inhalation Exposures

Potential health impacts from acute, one-hour exposures were estimated using acute

reference exposure levels (RELs). An REL is a concentration in air at or below which no

adverse health effects are anticipated for a specified exposure duration. RELs are based on the

most sensitive, relevant, adverse health effect reported in the medical and toxicological literature.

They are designed to protect the most sensitive individuals in the population by the inclusion of

margins of safety. Acute RELs used in the present risk analysis were obtained from the “Air

Toxics Hot Spots Program Risk Assessment Guidelines, Part I: The Determination of Acute

Reference Exposure Levels for Airborne Toxicants” (OEHHA, 1999a). As mandated by state

legislation, these guidelines underwent public and scientific peer review prior to approval by the
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

4

Scientific Review Panel and adoption by OEHHA (Senate Bill 1731, Statutes of 1992, Ch. 1162

of the California Health and Safety Code).

In the absence of adopted acute RELs, OEHHA calculated draft ‘health protective

concentrations’ following the adopted methodology for developing acute RELs. Details on the

methodology are provided in OEHHA (1999a).

3.1.2.2. Annual Average Inhalation Exposure Concentrations

Potential health impacts from chronic inhalation exposures were estimated using several

types of health assessment values.

a) U.S. EPA’s Reference Concentrations (RfCs). U.S. EPA has developed reference

concentrations (RfC) for many airborne toxicants. An RfC is defined by U.S. EPA as “an

estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation

exposure to the human population (including sensitive subgroups) that is likely to be without an

appreciable risk of deleterious noncancer effects during a lifetime.”

b) Proposed Chronic Reference Exposure Levels. In the absence of a U.S. EPA RfC,

OEHHA used the proposed chronic reference exposure levels currently being developed by the

Air Toxics Hot Spots Program risk assessment guidelines process. These values, as well as the

methodology used to develop them, are in the process of undergoing public and scientific peer

review. The methodology and proposed values are described in the “Air Toxics Hot Spots

Program Risk Assessment Guidelines, Part III: Technical Support Document for the

Determination of Noncancer Chronic Reference Exposure Levels” available on our web page

(www.oehha.ca.gov).

c) Reference Exposure Levels for Toxic Air Contaminants. OEHHA has developed RELs

for some chemicals evaluated in the Toxic Air Contaminant (TAC) program, mandated by

Assembly Bill 1807 (California Health and Safety Code 39660 et seq.) These numbers

underwent public and scientific peer review. One chemical in the present analysis, acetaldehyde,

has an REL that was developed under the TAC process.

In the absence of a U.S. EPA RfC, a proposed chronic REL, or an REL developed under the

TAC process, OEHHA calculated draft health protective concentrations using the chronic REL

methodology.
DRAFT OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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Table 1. Health Assessment Values and Draft “Health Protective Concentrations” (HPCs)

Non-cancer Cancer

1-hour

(mg/m3)

Annual Average

(mg/m3)

Unit risk

(mg/m3)

-1

Air concentration

corresponding to10-6

lifetime risk (mg/m3)

Acetaldehyde 115

(65 ppb)

[draft HPC]

9

(5 ppb)

[TAC]

2.7 E-6

(4.8 E-6 ppb-1)

[TAC]

3.7 E-1

(2.1 E-1 ppb)

Benzene 1300

(400 ppb)

[acute REL]

60

(20 ppb)

[proposed chronic REL]

2.9 E-5

(9.3 E-5 ppb-1)

[TAC]

3.5 E-2

(1.1 E-2 ppb)

Butadiene 310

(140 ppb)

[draft HPC]

8

(4 ppb)

[U.S. EPA RfC]

1.7 E-4

(3.7 E-4 ppb-1)

[TAC]

5.9 E-3

(2.7 E-3 ppb)

Ethanol 100,000

(53,000 ppb)

[draft HPC]

100,000

(53,000 ppb)

[draft HPC]

No evidence of carcinogenicity by inhalation

Formaldehyde 94

(76 ppb)

[acute REL]

3

(2 ppb)

[proposed chronic REL]

6.0 E-6

(7.0 E-6 ppb-1)

[TAC]

1.7 E-1

(1.4 E-1 ppb)

MTBE 25,000

(7000 ppb)

[draft HPC]

3000

(800 ppb)

[U.S. EPA RfC]

2.6 E-7

(9.3 E-7 ppb-1)

[TAC]

3.9 E0

(1.1 ppb)

PAN 8.8

(1.8 ppb)

[draft HPC]

3.2

(0.6 ppb)

[draft HPC]

No evidence of carcinogenicity / inadequate data

Draft HPC: health protective concentration; In the absence of adopted health assessment values OEHHA developed draft numbers

for use in this analysis. The basis of these numbers is described in Appendix A in the toxicity summaries. These numbers are

not in regulation.

TAC: toxic air contaminant; peer-reviewed value developed under the TAC program mandated by AB 1807

Acute REL: acute reference exposure level; peer-reviewed value developed as part of the legislatively mandated Air Toxics Risk

Assessment Program risk assessment guidelines process (SB 1731; Statutes of 1992; California Health and Safety Code, Chapter

1162)

Proposed chronic REL: chronic reference exposure level; currently being developed as part of the legislatively mandated Air Toxics

Risk Assessment Program risk assessment guidelines process (SB 1731; Statutes of 1992; California Health and Safety Code,

Chapter 1162); these numbers are currently undergoing various stages of a scientific peer review and public comment process.
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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Table 2. Health Assessment Values for the Criteria Air Pollutants

1 hour 8 hour 24 hour Annual Average

Carbon monoxide 23000 mg/m3 (20 ppm)

[acute REL; CA AAQS]

10,000 mg/m3 (9.0 ppm)

[CA and federal AAQS]

NOX 470 mg/m3 (0.25 ppm)

[acute REL; CA AAQS]

100 mg/m3 (0.053 ppm)

[federal AAQS]

Ozone 180 mg/m3 (0.09 ppm)

[acute REL; CA AAQS]

157 mg/m3 (0.08 ppm)

[federal AAQS]

Particulate Matter

 < 10 microns (PM10)

50 mg/m3

[CA AAQS]

30 mg/m3

[CA AAQS]

Acute REL: Acute Reference Exposure Level CA AAQS: California Ambient Air Quality Standard

Federal AAQS: Federal Ambient Air Quality Standard

3.2. Values for Assessing Potential Health Impacts from

Exposure

via Drinking Water

3.2.1. Public Health Goals (PHGs)

The PHG describes concentrations of contaminants in drinking water at which adverse health

effects are not expected to occur, even over a lifetime of exposure. PHGs have been developed

by OEHHA under the California Safe Drinking Water Act of 1996 (amended Health and Safety

Code, Section 116365). PHGs are based solely on scientific and public health considerations,

unlike many other state and federal drinking water standards which take into account other

considerations (e.g., technological feasibility and economic factors).

Table 3. Health Assessment Values and Draft “Health Protective Concentrations” for Assessing Potential

Health Impacts of Ethanol in Gasoline – Oral exposures from Drinking Water.

Health Assessment Value Endpoint Source Reference

Benzene 1.4  ́ 10-4 mg/L (0.14 ppb) cancer draft public health goal OEHHA (1999c)

Ethanol 1100 mg/L (1.1  ́ 106 ppb) noncancer draft HPC ---

Methyl t-butyl

ether (MTBE)

0.013 mg/L (13 ppb) cancer public health goal OEHHA (1999d)

Toluene 0.150 mg/L (150 ppb) noncancer public health goal OEHHA (1999e)

Xylenes 1.8 mg/L (1800 ppb) noncancer public health goal OEHHA (1997)

Public Health Goal (PHG): developed under the California Safe Drinking Water Act of 1986 (amended Health and Safety Code,

Section 116365)

Draft HPC: health protective concentration; In the absence of adopted health assessment values OEHHA developed draft numbers

for use in this analysis. The basis of these numbers is described in Appendix A in the toxicity summaries. These numbers are

not in regulation.
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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4. Exposure Assessment: Sources of Exposure

Data

The CARB conducted modeling analyses of the air quality impacts of use of one fuel versus

another. The South Coast airshed was selected as the basis of their modeling efforts since the

South Coast is a severely impacted area of the State and one which has been extensively studied.

The CARB analysis includes consideration of the changes in ambient air concentrations of

specific toxic components of exhaust, evaporative components, and subsequent reaction products

that would result from substituting ethanol-blended gasoline for gasoline blended with MTBE.

The modeled air concentrations incorporate all sources of emissions within the South Coast

airshed, including stationary source emissions, mobile source emissions and background

emissions. However, stationary source and background emissions are not expected to change

between the various fuel scenarios. As noted above, the fuels modeled include the current

MTBE formulation, two formulations containing ethanol, and a formulation containing no

oxygenate. These were considered in exposure scenarios based on the predicted emissions

inventory for the year 2003. A scenario of the 1997 emissions inventory and MTBE-containing

fuel was used to calibrate the model against actual measured data for that year. The model

predictions of one-hour and 24-hour peak concentrations of pollutants are worst case estimates,

but the population-weighted annual averages are best estimates calibrated against actual

measurements for 1997, the baseline year. CARB’s modeling analysis is described in more

detail in their report and the accompanying appendices of this document. CARB developed

speciation profiles of volatile organic compounds (VOC) for each fuel under varying conditions

(e.g., start exhaust, hot stabilized exhaust, etc.). The modeling results provide one-hour peak

concentrations for all compounds, eight-hour concentrations for ozone and CO, 24-hour average

concentrations for PM10, and population-weighted annual average concentrations for all

compounds of interest. These modeled air concentrations are summarized in Table 4 and form

the basis of the health impacts analysis. The concentrations are input into simple arithmetic

equations to estimate health risks.

As shown in Table 4, measurable air concentrations of ethanol are present even under the

non-ethanol-containing fuel scenarios. These ethanol emissions result primarily from stationary

sources. However, there are no detectable levels of MTBE under the non-MTBE-containing fuel

scenarios because stationary source emissions of MTBE are negligible and result in nondetectable air concentrations of the chemical.

The SWRCB contracted with Lawrence Livermore National Laboratories to model a variety

of scenarios related to release of ethanol-containing gasoline onto soil or into surface waters.

The main purpose of the modeling is to estimate potential water quality impacts of using ethanol

as an oxygenate in gasoline. The modeling focused on predicting the movement of ethanol

through the soil and into groundwater as well as the effects ethanol may have on the movement

of other gasoline constituents (primarily benzene, toluene, and xylenes; also referred to as

BTEX) through soil and into groundwater. Although the modeling analyses are not yet

complete, information to date indicates that ethanol readily undergoes microbial degradation in

the environment. This is in contrast to MTBE, which is resistant to microbial degradation. As a

result, it appears unlikely that ethanol will contaminate groundwater to any degree approaching a

public health concern. At this time, OEHHA is awaiting results of the modeling being conducted
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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on the effects of ethanol on the movement of other gasoline constituents (BTEX). The results of

the modeling will be used to ascertain whether the probability of well-water contamination by

BTEX will increase, decrease, or stay the same relative to baseline MTBE-containing fuels. If

possible, we may be able to obtain modeled concentrations of BTEX and ethanol to compare to

existing PHGs or estimated health-protective concentrations as described in the following

section.
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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Table 4. Atmospheric Concentration Estimates: Range of Predicted 1997 and 2003 Air Quality for the South

Coast Air Basina

1997

MTBE

2003

MTBE

2003

Et2%

2003

Et3.5%

2003

Non-Oxy

Acetaldehyde (ppb)

Population-Weighted Annual Exposure

Upper 1.8 1.6 1.6 1.8 1.6

Lower 1.8 1.5 1.5 1.7 1.5

Maximum Daily Average

Upper 6.2 6.2 6.2 6.2 6.2

Lower 5.1 5.1 5.1 5.1 5.1

Maximum 1 Hour Average

Upper 17.7 16.7 16.9 17.1 16.9

Lower 13.8 13.1 13.2 13.4 13.2

Benzene (ppb)

Population-Weighted Annual Average

Upper 1.19 0.80 0.78 0.81 0.76

Lower 1.07 0.72 0.70 0.73 0.69

Maximum Daily Average

Upper 9.5 6.8 6.5 6.8 6.4

Lower 7.4 5.3 5.1 5.3 4.9

Maximum 1 Hour Average

Upper 22.4 14.3 14.3 14.3 14.3

Lower 11.6 7.4 7.4 7.4 7.4

Butadiene (ppb)

Population-Weighted Annual Average

Upper 0.36 0.20 0.20 0.20 0.20

Lower 0.34 0.19 0.19 0.19 0.19

Maximum Daily Average

Upper 2.9 1.2 1.2 1.2 1.2

Lower 2.0 0.8 0.8 0.8 0.8

Maximum 1 Hour Average

Upper 6.7 3.4 3.4 3.4 3.4

Lower 3.1 1.6 1.6 1.6 1.6

Ethanol (ppb)

Population-Weighted Annual Average

Best 5.4 5.1 7.6 8.8 5.1

Maximum Daily Average

Upper 51 49 71 81 49

Lower 47 45 64 75 45

Maximum 1 Hour Average

Upper 108 101 145 165 101

Lower 78 74 114 140 74
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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Table 4 (continued). Atmospheric Concentration Estimates: Range of Predicted 1997 and 2003 Air Quality

for the South Coast Air Basina

1997

MTBE

2003

MTBE

2003

Et2%

2003

Et3.5%

2003

Non-Oxy

Formaldehyde (ppb)

Population-Weighted Annual Average

Upper 4.7 4.2 4.1 4.1 4.0

Lower 4.7 4.1 4.0 4.0 4.0

Maximum Daily Average

Best 14.0 12.2 11.8 12.1 11.7

Maximum 1 Hour Average

Upper 37.8 38.3 37.8 38.1 37.8

Lower 20.3 20.6 20.3 20.5 20.3

MTBE (ppb)

Population-Weighted Annual Average

Upper 3.9 2.6 0 0 0

Lower 3.6 2.4 0 0 0

Maximum Daily Average

Upper 29 20 0 0 0

Lower 13 9 0 0 0

Maximum 1 Hour Average

Upper 67 46 0 0 0

Lower 19 13 0 0 0

PAN (ppb)b

Maximum Daily Average

Upper

Lower

5.0

2.5

4.8

2.4

4.8

2.4

4.9

2.4

4.7

2.4

Maximum 1 Hour Average

Upper

Lower

10.0

5.0

9.5

4.8

9.3

4.7

9.5

4.8

9.1

4.5
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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Table 4 (continued). Atmospheric Concentration Estimates: Range of Predicted 1997 and 2003 Air Quality

for the South Coast Air Basina

1997

MTBE

2003

MTBE

2003

Et2%

2003

Et3.5%

2003

Non-Oxy

Carbon Monoxide (ppm)

Maximum 8 Hour Average

Best 17.5 14.3 14.3 13.4 14.7c

Maximum 1 Hour Average

Best 22.5 19.2 19.2 18.0 19.7c

Nitrogen Dioxide (ppm)

Maximum Annual Average

Best 0.043 CARB reported, “No difference expected among 2003 scenarios” d

Maximum Daily Average

Best 0.117 0.098 0.097 0.097 0.097

Maximum 1 Hour Average

Best 0.255 0.235 0.235 0.235 0.235

Ozone (ppm)

Maximum 8 Hour Average

Best 0.206 0.196 0.196 0.196 0.196

Maximum 1 Hour Average

Best 0.244 0.230 0.228 0.228 0.228

Particulate Matter (10 microns or less) (mg/m3)

Maximum Annual Geometric Mean

Best 56 CARB reported, “No difference expected among 2003 scenarios” d

Maximum Daily Average

Best 227 CARB reported, “No difference expected among 2003 scenarios” d

a Source: Table 4.6 of “Staff Report: Air Quality Impacts of the Use of Ethanol in California Reformulated Gasoline. November 18,

1999. California Air Resources Board, Cal/EPA”

b A population-weighted annual average for PAN was not determined because consistent long-term measurements of atmospheric

PAN have not been performed. See CARB report for details.

c This apparent increase is a function of the emission assumptions. Due to the wintertime oxygenate requirement for the SoCAB, CO

concentrations within the nonattainment area of Los Angeles County will not differ from the 2003 MTBE baseline.

d No significant change compared to 1997 MTBE-fuel scenario. See CARB report for details.
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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5. Methodology Used for Quantifying Cancer

and Noncancer Risks

Risk characterization is the process of integrating data on exposure with dose-response in

order to estimate public health impacts. In quantifying risks of exposure, cancer and noncancer

endpoints are considered separately. Please refer to the toxicity summaries in Appendix A for

further details on estimating cancer and noncancer risks for individual chemicals.

5.1. Estimating Cancer Risk

Typically, carcinogenesis is treated as a “nonthreshold” toxicological phenomenon. In other

words, there is some finite risk to any finite dose. It may be so small as to be indistinguishable

from zero at very low doses. In order to estimate cancer risk, we multiply the unit risk factor by

the modeled concentration in air to obtain a unitless probability of cancer occurring in a

population thus exposed.

Risk = concentration × (URF or potency slope)

So, for example, if the unit risk factor is 1 × 10-6 for chemical “X”, and the concentration of

chemical “X” is 5 μg/m3, then the risk is calculated as :

Risk = [(1 × 10-6) (μg/m3

)

-1] × 5 μg/m3

 = 5 × 10-6

The cancer risks thus estimated reflect high-end estimates (usually a 95% upper confidence

limit or UCL95) of the potential cancer cases in a population exposed to chemical “X” at

5 μg/m3

 over a lifetime. In other words, there is the potential for five extra cancer cases to occur

over a 70 year period in a population of one million persons exposed to that level of chemical

“X”.

In cases where there is exposure to multiple carcinogens, the risk of each carcinogen is

added. The implicit assumption is that the effect on cancer risk in the population exposed to

multiple carcinogens is additive. It is possible that some carcinogens might be synergistic and

some antagonistic, although at low exposure levels these mechanisms may be unimportant.

5.2. Estimating Noncancer Risk

Noncancer health endpoints are assumed to have a threshold for effect. If the exposure is

below the individual’s threshold for effect, then no adverse impact would be expected. To

quantify potential noncancer health impacts resulting from exposure to hazardous substances, a

hazard index approach is used. In using this approach, measured or modeled exposure

concentrations are compared to calculated health assessment values such as the Reference

Exposure Level (REL). The Hazard Quotient (HQ) for a chemical is the ratio of the modeled

concentration in air to the REL. If the HQ exceeds one, a ‘red flag’ is raised with regard to

exposure to that chemical and possible adverse health impacts. Exceedance of an HQ of one
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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does not necessarily mean that a health impact will occur. It implies that the margin of safety

built into the REL is being eroded. The higher the ratio, the closer the exposure is to an adverse

level. It is generally impossible to calculate the exact concentration at which anyone in a diverse

population would respond. Interindividual differences in response and limited information on

the toxicant preclude such a determination. Uncertainty factors are included in the calculation of

the RELs to protect sensitive members of the population.

To assess the cumulative impact of several chemicals present at the same time, it is important

to consider the interaction of the effects of the toxicants. Unless specific information is available

to the contrary, the interaction of two or more chemicals that affect the same target organ is

assumed to be additive. An underlying issue in chemical interactions and additivity is the

concept of threshold. Exposure to a single chemical may not result in a toxic response if it is

below the threshold necessary to elicit a response. However, simultaneous exposure to two or

more chemicals that impact the same target organ at sub-threshold concentrations may result in a

toxic response. This is taken into account by adding the individual HQs for chemicals that

impact the same target organ or system. Thus, if more than one toxicant is present that impacts

the same target organ or system (e.g., respiratory system, cardiovascular system), then the HQ

for individual compounds is added to produce the Hazard Index (HI). As such, the hazard index

approach assumes that multiple sub-threshold exposures to chemicals acting on the same target

organ could result in an overall risk of developing adverse effects. This may underestimate the

effect in the cases in which interactions are synergistic, or overestimate it if the interactions are

not additive or are antagonistic.
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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6. Risk Characterization

6.1. Inhalation – Cancer and Noncancer Effects

The following section refers to data presented in Tables 5a-c. Please refer to the toxicity

summaries in Appendix A for relevant citations and information pertaining to the basis and the

development of the health assessment values for individual chemicals.

6.1.1. Acetaldehyde

The lifetime cancer risk is the toxicological endpoint of concern for exposure to acetaldehyde

in the South Coast Air Basin. Toxic endpoints may include nasal and pulmonary cancers, with a

cancer unit risk value of 2.7 × 10-6 (μg/m3)

-1 or 4.8 × 10-6 ppb-1. Several sources of uncertainty

result in a lower level of confidence in this estimate for acetaldehyde than for some of the other

carcinogenic potency estimates, for example, the benzene and butadiene cancer risk estimates.

The sources of uncertainty are similar to those facing other cancer potency estimates. They

include reliance on animal studies due to the lack of human data, and the five orders of

magnitude extrapolation from experimental animal exposure concentrations to current ambient

levels. In the case of acetaldehyde, the extensive metabolism of the compound in vivo (and its

occurrence as a normal intermediary metabolite) is an additional source of uncertainty with

respect to the standard assumption in risk assessment that the dose-response curve is linear down

to the low ambient levels of the compound.

The upper bound estimate of the cancer risk resulting from exposure to the maximal

predicted levels of acetaldehyde over a 70 year lifespan is seven to nine excess cancer cases per

million people exposed. The real risk may in fact be considerably lower than this upper bound

estimate. There are increased ambient concentrations of acetaldehyde from the ethanol-based

fuel containing 3.5% oxygen, compared to the other formulations evaluated for the year 2003.

This results in an increase of up to two in a million excess lifetime cancer cases in the upper

bound estimate. However, in view of the uncertainties both in the emission and exposure

predictions, and in the acetaldehyde lifetime cancer risk estimate, this predicted increase in risk

may be regarded as of marginal significance when comparing the other consequences of the

different fuel formulations. None of the predicted ambient levels of acetaldehyde for the year

2003 exceeds the levels in the 1997 model.

The acute (one-hour maximal average) and chronic (maximum annual exposure) noncancer

Hazard Quotients (HQs) for acetaldehyde generated by each of the fuel scenarios are well below

one. In general, the air concentrations are three- to five-fold below the reference exposure levels

and there is little difference in HQ values among the five fuel types. Toxicological endpoints

considered include eye, skin, and respiratory tract irritation with acute exposure, and

inflammation of the respiratory tract and degeneration of the olfactory epithelium with chronic

exposure.
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6.1.2. Benzene

The lifetime cancer risk is the toxicological endpoint of concern for exposure to benzene in

the South Coast Air Basin. Health effects other than cancer are not expected to occur at maximal

ambient levels. The primary toxic endpoint in humans is acute myelogenous leukemia, but

strong evidence exists to suggest that benzene causes other forms of leukemia as well (OEHHA,

1999c). The current cancer unit risk value for California, 2.9 × 10-5 (μg/m3)

-1 or 9.3 × 10-5 ppb-1,

is based on total leukemia (i.e. all forms of leukemia as a related class of diseases). There is a

moderate to high level of confidence in the estimate of this value. Principally, there exists

sufficient evidence to consider benzene a carcinogen in both humans and experimental animals.

The cancer risk value is the upper 95 percent confidence level estimate from the analysis of

human data and falls within the range of estimates derived from numerous epidemiological and

animal studies. However, the approximate five orders of magnitude extrapolation from human

occupational exposure concentrations to current ambient levels represent a major source of

uncertainty for the benzene cancer risk estimate. Although some experts have postulated that the

mechanism by which benzene causes leukemia may have a threshold, there are also substantial

reasons for considering that benzene is acting as a nonthreshold genotoxic carcinogen (reviewed

in OEHHA, 1999c). Based on this latter interpretation, benzene is treated as a substance without

a carcinogenic threshold in humans (OEHHA, 1999c; U.S. EPA, 1999).

Comparing the 1997 fuel scenario to the year 2003 formulations, the upper bound estimate of

the cancer risk resulting from exposure to the maximal predicted levels of benzene over a 70 year

lifespan is expected to drop from 110 to 75 or less excess cancer cases per million people

exposed. Given the uncertainty in the cancer risk estimate, the differences in cancer risks

between the various year 2003 fuel scenarios are small and insignificant.

The most sensitive toxicological endpoint under acute exposures may include reduced birth

weights in newborns. Chronic exposure and high acute exposure to benzene may result in

hematotoxicity, including aplastic anemia. However, with acute and chronic noncancer HQs

generated for benzene by each of the five fuel scenarios well below one, these noncancer health

effects are not expected to occur even at maximum ambient levels. The upper bound

concentrations in air are between 17- and 25-fold below the REL and there is essentially no

difference in HI values among the year 2003 formulations.

6.1.3. Butadiene

The lifetime cancer risk is the toxicological endpoint of concern for exposure to butadiene in

the South Coast Air Basin. Butadiene has been shown to induce cancers in animals at multiple

sites including, heart, lung, mammary gland, ovaries, liver, pancreas, Zymbal gland, thyroid,

testes, and hematopoietic system. The cancer unit risk value is 1.7 × 10-4 (μg/m3

)

-1 or

3.7 x 10-4 ppb-1. There is a moderate level of confidence in the estimate of this value. Recent

epidemiological studies suggest a connection between excess cases of leukemia and lymphoma

and butadiene exposure, although this provides only limited evidence to support the carcinogenic

effects observed in experimental animals. Mice are known to develop lymphomas following

butadiene exposure, although this has not been observed in the rat. This interspecies difference

is a significant source of uncertainty in the risk estimate, and may reflect differences seen

between mice and rats regarding butadiene metabolism. Another uncertainty results from the

necessity to extrapolate from experimental animal exposure concentrations to current ambient
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levels. However, the evidence on metabolism and carcinogenicity suggests that butadiene is a

genotoxic carcinogen acting via metabolically generated reactive intermediates. Hence, no

threshold is thought to exist for this substance.

Comparing the1997 fuel scenario to the year 2003 formulations, the upper end estimate of

the cancer risk resulting from exposure to the maximal predicted levels of butadiene over a 70

year lifespan is expected to drop from 130 to about 74 excess cancer cases per million people

exposed. The real risks may be lower than these upper bound estimates. Given the uncertainty

in the cancer risk estimates, the differences in cancer risks between the various year 2003 fuel

scenarios are small and likely to be of little significance.

The most sensitive toxicological endpoint under acute exposures may include reduced birth

weights in newborns. Chronic exposure to butadiene may result in ovarian atrophy. However,

with acute and chronic noncancer HQs generated for butadiene by each of the five fuel scenarios

are well below one, these noncancer health effects are not expected to occur even at maximal

ambient levels. There is essentially no difference in HQ values among the year 2003

formulations, though the year 2003 formulations have significantly lower chronic HQs than the

1997 formulation. The upper and lower bound one-hour average concentrations are between 20-

and 100-fold below the acute REL.

6.1.4. Ethanol

Health effects due to ethanol exposure under any of the five fuel scenarios are not expected

to occur at modeled ambient levels. There is no evidence that ethanol is carcinogenic via the

inhalation route. Exposure to high concentrations of ethanol vapor may result in transient

irritation to eyes and the respiratory system under either acute or chronic conditions. However,

the acute and chronic noncancer HQs generated for ethanol by each of the five fuel scenarios are

0.002 or less, indicating that modeled concentrations are at least 500-fold below the HPCs.

As discussed in Appendix A, OEHHA concluded that ethanol exposure via the inhalation

route at the low ambient concentrations predicted by CARB is unlikely to present a carcinogenic

hazard. However, in order to further explore the possible impact of atmospheric pollution by

ethanol, OEHHA evaluated the implications of a proposed unit risk factor (R. Wilson, 1999;

comment on a draft of this document) and found that even if ethanol were regarded as a human

carcinogen by the inhalation route, with linear low-dose response, the cancer risks predicted on

this basis from ethanol are negligible. This analysis is described in detail in the attached listing

of public comments.

6.1.5. Formaldehyde

The lifetime cancer risk is the toxicological endpoint of concern for exposure to

formaldehyde in the South Coast Air Basin. The primary toxic endpoint is nasal cancer, but may

also include other respiratory tract cancers. The cancer unit risk is 6.0 × 10-6 (μg/m3

)

-1 or

7.0 × 10-6 ppb-1. The sources of uncertainty in this estimate are similar to those facing other

cancer potency estimates. They include reliance on animal studies due to insufficient human

data, and three to four orders of magnitude extrapolation from experimental animal exposure

concentrations to current annual average exposure levels. Another uncertainty involves crossspecies scaling calculations. The evidence indicates formaldehyde is a contact carcinogen (i.e.,

formaldehyde generally reacts with the first tissues it contacts) so that whole-body scaling
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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factors may not be appropriate. Because the formaldehyde cancer unit risk is based on studies in

rats, there is uncertainty in extrapolating to humans due to potentially significant differences in

the anatomy and physiology of the respiratory systems between rats and humans.

Comparing the 1997 fuel scenario to the year 2003 scenarios, the upper bound estimate of the

cancer risk resulting from exposure to the maximal predicted levels of formaldehyde over a 70

year lifespan is expected to drop from 33 to about 28-29 excess cancer cases per million people

exposed by 2003. There is no apparent difference between year 2003 fuel formulations

regarding cancer risk from formaldehyde.

The chronic (maximum annual exposure) noncancer HQ generated by the 1997 fuel scenario

is 2.4. The 2003 fuel scenarios have lower HQs, but indicate that the concentrations of

formaldehyde are almost two-fold above the REL. There is no apparent difference between fuel

formulations for year 2003 of possible chronic health effects of formaldehyde. Toxicological

endpoints include eye and respiratory system irritation. It is possible that some sensitive

individuals may develop these chronic adverse effects at the maximal predicted annual exposure.

Simultaneous exposure to other sensory irritants, such as acetaldehyde, may exacerbate the eye

and respiratory irritation caused by formaldehyde (see section 6.4). However, it should be noted

that the proposed chronic REL is undergoing revision and the value may change. The acute

health effects from formaldehyde, primarily due to eye irritation, are not anticipated to occur at

the predicted maximal ambient levels. The upper bound maximum one-hour average

concentrations for all five fuel scenarios were two-fold below the acute REL.

Significant indoor exposures to formaldehyde are known to occur. However, the emission

estimates determined in this report for all pollutants, including formaldehyde, do not address

potential additional exposure to indoor sources of formaldehyde. Unlike the formaldehyde TAC

document, the estimated cancer risk and noncancer hazards reported here do not reflect the

potential for indoor exposure to formaldehyde.

6.1.6. Methyl t-Butyl Ether (MTBE)

The lifetime cancer risk is the toxicological endpoint of concern for exposure to MTBE in the

South Coast Air Basin. Toxic endpoints in animal studies included leukemia, lymphoma, and

testicular, kidney, and liver cancer. The cancer unit risk estimate is 2.6 × 10-7 (μg/m3)

-1 or

9.3 × 10-7 ppb-1. The sources of uncertainty include those facing other cancer potency estimates,

such as reliance on animal studies due to the lack of human data, and the extrapolation from

experimental animal exposure concentrations to current ambient levels. Some additional sources

of uncertainty apply in this particular case since the mechanism of action of MTBE as a

carcinogen is unknown. The estimate therefore relies on health protective default assumptions as

to the applicability of the findings in animals to humans, resulting in the use of a non-threshold

model for the low-dose region.

The upper bound estimate of the cancer risk resulting from exposure to the annual average

levels of MTBE predicted in the 1997 scenario, over a 70 year lifespan, is 3.6 excess cancer

cases per million people exposed. In the 2003 scenario with the same MTBE-containing fuel,

the resulting cancer risk estimate of 2.4 excess cancer cases per million people exposed is

approximately one-third lower. The cancer risk via inhalation of MTBE is zero for scenarios

where the fuel formulation does not contain MTBE.
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The acute and chronic noncancer HQs generated by each of the MTBE-containing fuel

scenarios are at least 0.01, indicating that modeling concentrations are at least 100-fold below the

RELs. Noncancer health effects due to acute or chronic MTBE exposure are not expected to

occur at maximal ambient levels. The most sensitive toxicological endpoints for acute inhalation

exposure may include eye irritation, respiratory irritation and CNS effects (headache, nausea,

vomiting, dizziness, and disorientation). The most sensitive toxicological endpoints for chronic

exposure may include eye irritation, kidney damage, and CNS depression.

6.1.7. Peroxyacetyl Nitrate (PAN)

The acute noncancer HQs for PAN based on the results of the air modeling are above the

threshold at which toxic effects may occur. Acute noncancer effects are the toxicological

endpoints of concern for this pollutant in the South Coast Air Basin; the most sensitive of these

is eye irritation. The one-hour maximum predicted HQ is 5.5 or less under all fuel scenarios. It

appears that none of the scenarios for the year 2003 involves an exacerbation of the adverse

health impact of PAN compared to the 1997 data. While these HQs are above one, it should be

recognized that the air modeling results for short-term exposures reflect unfavorable

meteorology. However, it is possible that some sensitive individuals may develop acute adverse

effects at the maximum predicted exposure. Simultaneous exposure to other sensory irritants,

such as formaldehyde, may exacerbate the eye irritation caused by PAN. As mentioned above,

the CARB notes that they have much more confidence in the relative values than the absolute

values of concentrations of the modeled chemicals.

Notably, there has been a consistent downward trend in the observed average acute PAN

concentrations in the South Coast Air Basin. Twenty-four hour average PAN concentrations

have declined from 15-20 ppb in the late 1960s, to 5-12 ppb in 1985-1990 and 2-5 ppb in 1993.

Therefore, it may be concluded that the irritant effects due to exposure to PAN have decreased

proportionally in the South Coast Air Basin since the 1960s.

A population-weighted annual average exposure to PAN has not been determined because

consistent long-term measurements of atmospheric PAN have not been measured. Therefore, a

chronic HQ cannot be adequately determined. The most sensitive endpoint from chronic

exposure to PAN may include inflammation, epithelial metaplasia and hyperplasia in the

respiratory tract.

Currently, there is inadequate evidence to determine if PAN is carcinogenic in either

experimental animals or humans.
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Table 5a. Range of Estimated Maximum Noncancer Hazard Quotients (HQ) for Various Scenarios in the

South Coast Air Basin

1997

MTBE

2003

MTBE

2003

Et2%

2003

Et3.5%

2003

NonOxy

Acetaldehyde

Upper 0.4 0.3 0.3 0.4 0.3

Chronic HQ Lower 0.4 0.3 0.3 0.3 0.3

Upper 0.3 0.3 0.3 0.3 0.3

Acute HQ Lower 0.2 0.2 0.2 0.2 0.2

Benzene

Upper 0.06 0.04 0.04 0.04 0.04

Chronic HQ Lower 0.05 0.04 0.04 0.04 0.03

Upper 0.06 0.04 0.04 0.04 0.04

Acute HQ Lower 0.03 0.02 0.02 0.02 0.02

Butadiene

Upper 0.09 0.05 0.05 0.05 0.05

 Chronic HQ Lower 0.09 0.05 0.05 0.05 0.05

Upper 0.05 0.02 0.02 0.02 0.02

 Acute HQ Lower 0.02 0.01 0.01 0.01 0.01

Ethanol

Best 0.0001 0.0001 0.0001 0.0002 0.0001

 Chronic HQ

Upper 0.002 0.002 0.003 0.003 0.002

 Acute HQ Lower 0.001 0.001 0.002 0.003 0.001

Formaldehyde

Upper 2.4 2.1 2.1 2.1 2.0 Chronic HQ Lower 2.4 2.1 2.0 2.0 2.0

Upper 0.5 0.5 0.5 0.5 0.5 Acute HQ Lower 0.3 0.3 0.3 0.3 0.3

MTBE

Upper 0.005 0.003 0.0 0.0 0.0 Chronic HQ Lower 0.005 0.003 0.0 0.0 0.0

Upper 0.01 0.007 0.0 0.0 0.0 Acute HQ Lower 0.003 0.002 0.0 0.0 0.0

PAN*

Upper 5.5 5.3 5.2 5.3 5.1 Acute HQ

Lower 2.7 2.7 2.6 2.7 2.5

* A population-weighted annual average for PAN was not determined because consistent long-term measurements of

 atmospheric PAN have not been performed. See CARB report for details.
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Table 5b. Range of Estimated Maximum Noncancer Hazard Quotients (HQ) for Various Scenarios in the

South Coast Air Basin – Criteria Air Pollutants

1997

MTBE

2003

MTBE

2003

Et2%

2003

Et3.5%

2003

NonOxy

Carbon Monoxide

Acute 8 hour HQ 1.9 1.6 1.6 1.5 1.6

Acute 1 hour HQ 1.1 1.0 1.0 0.9 1.0

Nitrogen Dioxide

Chronic HQ 0.8 concentrations not estimated by CARB since no significant

change in Maximum 1-Hour*

Acute 1 hour HQ 1.0 0.9 0.9 0.9 0.9

Ozone

Acute 8 hour HQ 2.6 2.5 2.5 2.5 2.5

Acute 1 hour HQ 2.7 2.6 2.5 2.5 2.5

Particulate Matter (PM10)

Chronic HQ 1.9

Acute 24 hour HQ 4.5

CARB reported, “No significant change expected among

2003 scenarios” for both annual and daily concentrations*

* compared to exposure estimates for the 1997 MTBE-fuel scenario (see CARB report for details)
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Table 5c. Range of Estimated Maximum Lifetime Cancer Risk Values for Various Scenarios in the South

Coast Air Basin

1997

MTBE

2003

MTBE

2003

Et2%

2003

Et3.5%

2003

NonOxy

Acetaldehyde

Upper 8.6 x 10-6 7.6 x 10-6 7.6 x 10-6 8.6 x 10-6 7.6 x 10 Lifetime -6

Cancer Risk Lower 8.6 x 10-6 7.2 x 10-6 7.6 x 10-6 8.1 x 10-6 7.2 x 10-6

Benzene

Upper 1.1 x 10-4 7.4 x 10-5 7.3 x 10-5 7.5 x 10-5 7.1 x 10 Lifetime -5

Cancer Risk Lower 1.0 x 10-4 6.7 x 10-5 6.5 x 10-5 6.8 x 10-5 6.4 x 10-5

Butadiene

Upper 1.3 x 10-4 7.4 x 10-5 7.4 x 10-5 7.4 x 10-5 7.4 x 10 Lifetime -5

Cancer Risk Lower 1.3 x 10-4 7.0 x 10-5 7.0 x 10-5 7.0 x 10-5 7.0 x 10-5

Formaldehyde

Upper 3.3 x 10-5 2.9 x 10-5 2.9 x 10-5 2.9 x 10-5 2.8 x 10 Lifetime -5

Cancer Risk Lower 3.3 x 10-5 2.9 x 10-5 2.8 x 10-5 2.8 x 10-5 2.8 x 10-5

MTBE

Lifetime Upper 3.6 x 10-6 2.4 x 10-6 0.0 0.0 0.0

Cancer Risk Lower 3.3 x 10-6 2.2 x 10-6 0.0 0.0 0.0
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6.2. Risk Characterization for Other Compounds of Concern:

Toluene, Xylenes, Isobutene, n-Hexane.

A number of compounds were evaluated for possible adverse health impacts, besides those

for which detailed atmospheric model data were developed by the CARB. In particular, the

toxicological properties of toluene, xylenes, isobutene and n-hexane were considered since they

have been identified as substantial fuel components. A detailed discussion of the potential

toxicity for each of these chemicals is summarized in Appendix A. CARB provided measured or

modeled concentrations of these compounds in the South Coast airshed for the year 1997 during

which MTBE-containing fuel was used.

In each of these cases the annual average concentrations found or estimated were

substantially below the chronic REL or other health protective concentrations, with a projected

HQ of 0.1 or less (see Table 6 for details). None of these materials is a suspected human

carcinogen. For acute exposures to toluene, m/p-xylene and o-xylene, the one-hour and 24-hour

peak concentrations were also substantially below the corresponding health risk values. No

acute health protective concentrations have been determined for isobutene and n-hexane, but

since the predicted concentrations for acute episodes did not exceed the chronic protective levels

for these compounds, no adverse acute health consequences are anticipated.

The emissions data and atmospheric model outputs for these compounds were not developed

using the 2003 scenario. However, it was anticipated that there would be little or no change

between the different fuel types, and a modest improvement relative to the 1997 (MTBE)

scenario. Since no plausible variations in the model output would alter the conclusion that these

compounds present no significant risk, it was not considered necessary to predict the 2003

outcomes in greater detail.

Table 6. Comparison of Estimated Maximum Pollutant Levels in California (based on South Coast Air Basin

Data for 1996-1997) and Health Assessment Values

Toluene

(ppbV)

m/p-Xylene

(ppbV)

o-Xylene

(ppbV)

Isobutene

(ppbV)

n-Hexane

(ppbV)

Annual Average *

Maximum Measured Value ** 5.1 2.2 0.77 --- ---

Projected Range of Maximum

based on CO levels

5.6-11.4 2.8-4.7 1.0 - 4.4 2.2 - 3.9 1.2 - 2.6

Chronic REL 100 170 170 1100 60

Maximum 1 hour Average

Extrapolated from Measured

24-Hour Maximum **

29.7 14.3 5.5 --- ---

Projected Range of Maximum

based on CO levels

51 - 103 25 - 45 8.8 - 40 22 - 35 11 - 23

Acute REL 9800 (6h) 5000 (0.5h) 5000 (0.5h) NA NA

* Overall Statewide Population-Weighted Annual Exposure typically would be between 1⁄2 and 3⁄4 of the Maximum

** There is currently some uncertainty in measurement techniques; actual values may be higher.
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6.3. Cumulative Cancer Impact of Multiple Chemical Exposures

The cumulative impact due to exposure to multiple cancer-causing chemicals is determined

by the addition of all the corresponding lifetime risks of the chemicals involved. The lifetime

risk is expressed as the estimated excess risk that results from lifetime exposure (i.e. 70 years) to

a specific air concentration of a cancer-causing chemical. Unlike the cumulative impact

methodology for noncancer toxicological endpoints, the lifetime risk from exposure to multiple

cancer-causing chemicals is assumed to be additive regardless of the toxicological endpoint or

target organ. This is because chemically induced cancer is considered predominantly a nonthreshold event that is irreversible once initiated and because the target tissue may vary from

species to species.

Table 7 displays 95 percent upper confidence limit estimates of lifetime cancer risk based on

the predicted exposure concentration of each chemical, and the aggregate lifetime risk

attributable to exposures to all these chemicals, for each fuel scenario in the South Coast Air

Basin. Risk estimates were calculated using the range of atmospheric concentration estimates

provided by CARB. These exposure estimates are best estimates of the population-weighted

annual average exposures, with variations in model assumptions as described earlier by CARB.

The last row displays the estimated range of excess cancer cases per million people that can be

expected from lifetime exposure to the aggregate of cancer-causing pollutants.

Comparison among the individual pollutants shows that, regardless of the fuel scenario,

benzene and butadiene are the major contributors to excess cancers due to airborne exposure to

cancer-causing pollutants in the South Coast Air Basin. The contribution of excess cancer cases

by acetaldehyde and MTBE by comparison is relatively minor. A small increase in acetaldehyde

concentration in the Et3.5% 2003 scenario has no effect on the overall cancer risk, due to the

lower potency of acetaldehyde compared to other pollutants such as benzene and butadiene, and

to minor reductions in butadiene- or MTBE-related risks relative to the other 2003 scenarios.

Comparing the 1997 fuel scenario to the year 2003 fuel scenarios, the upper bound estimate

of the excess cancer cases per million individuals is expected to drop from 270 - 290 to 170 - 190

excess cancer cases by 2003. There are very minor differences in the predictions for 2003 (170 -

180 excess cases per million for 2.5% ethanol and non-oxy fuels, compared to 180 - 190 for

3.5% ethanol and MTBE). But these appear to be much less than the uncertainty in the

estimates, indicating that there is no difference among the year 2003 fuel scenarios regarding

cancer risk. The conclusion that can be drawn from the cumulative exposure to airborne cancercausing pollutants in the South Coast Air Basin is that the reduction in excess cancers, from the

1997 fuel scenario to the 2003 fuel scenarios, results from expected reductions in overall

emissions, rather than a reduction in cancer causing emissions due to the use of any single fuel

scenario.
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Table 7. Lifetime Cancer Risk from Individual Chemicals and Cumulative Lifetime Cancer Risk for Each of

the Five Fuel Scenarios.

Chemical 1997

MTBE

2003

MTBE

2003

Et2%

2003

Et3.5%

2003

NonOxy

Upper 8.6 E-6 7.6 E-6 7.6 E-6 8.6 E-6 7.6 E-6 Acetaldehyde

Lower 8.6 E-6 7.2 E-6 7.6 E-6 8.1 E-6 7.2 E-6

Upper 1.1 E-4 7.4 E-5 7.3 E-5 7.5 E-5 7.1 E-5 Benzene

Lower 1.0 E-4 6.7 E-5 6.5 E-5 6.8 E-5 6.4 E-5

Upper 1.3 E-4 7.4 E-5 7.4 E-5 7.4 E-5 7.4 E-5 Butadiene

Lower 1.3 E-4 7.0 E-5 7.0 E-5 7.0 E-5 7.0 E-5

Upper 3.3 E-5 2.9 E-5 2.9 E-5 2.9 E-5 2.8 E-5 Formaldehyde

Lower 3.3 E-5 2.9 E-5 2.8 E-5 2.8 E-5 2.8 E-5

Upper 3.6 E-6 2.4 E-6 0 0 0 MTBE

Lower 3.3 E-6 2.2 E-6 0 0 0

Cumulative Lifetime Upper 2.9 E-4 1.9 E-4 1.8 E-4 1.9 E-4 1.8 E-4

Risk Lower 2.7 E-4 1.8 E-4 1.7 E-4 1.7 E-4 1.7 E-4

Excess Cancer Cases Upper 290 190 180 190 180

Per Million Individuals Lower 270 180 170 170 170

An inherent uncertainty resulting from addition of multiple lifetime cancer risks is that this

may underestimate the cancer risk in cases where the interactions are synergistic, or overestimate

the cancer risk in cases where the interactions are not additive or are antagonistic. Also, the

aggregate risk prediction may exaggerate the confidence bounds on the estimate, since it is

obtained by adding individual upper 95 percent confidence limits on the contributing risks.

Since it is not known how the various risks and the uncertainties in their estimates interact, it has

not been possible to allow for this effect.

The sources of uncertainty that are incorporated into the estimate of lifetime cancer risks,

such as reliance on animal data and extrapolation from experimental exposure concentrations to

ambient exposure concentrations, imply that the real aggregate risk may in fact be lower than the

upper bound estimates. On the other hand, the exposure concentrations provided by CARB’s

model that serve as the basis for the cancer calculations are population-weighted annual

averages. Certain individuals or communities located in areas where pollutant emissions are

concentrated (such as those near freeways or fuel storage and handling facilities) may experience

greater increments in risk from some fuel-related pollutants, whereas the impacts in other areas

may be less. As noted above, there is more confidence in the relative differences between fuels

than the absolute magnitude of the risk faced by the exposed population under the various

scenarios considered. Therefore, comparison of the aggregate cancer risks among the five fuel

scenarios gives a reasonably good indication of the relative impact of each fuel on the cancer risk

from airborne pollutants in the South Coast Air Basin.
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6.4. Cumulative Noncancer Impact of Multiple Chemical

Exposures

By definition, exposure to a single chemical in the air will not result in a toxic response if it

is below the threshold necessary to elicit a response. However, simultaneous exposure to two

similar chemicals at sub-threshold levels may result in a toxic response. Under the noncancer

cumulative impact methodology, the combined impact of several chemicals present at the same

time are assessed by assuming the interaction of the chemicals will be additive for a given

toxicological endpoint, unless information is available to the contrary.

The cumulative impact is determined by simply adding the HQs for chemicals that impact the

same target organ or system. If either the HQ for an individual chemical or the cumulative

hazard index (HI) for a particular toxicological endpoint exceeds one, the margin of safety

implicit in the REL is eroded. As noted in the introduction, this does not automatically imply

that adverse health effects will occur. Rather, it indicates that there is an increasing possibility

that more sensitive individuals may be affected. For the airborne pollutants of concern in the

South Coast Air Basin, cumulative HIs for a given toxicological endpoint can be determined

under each fuel scenario and for each predicted exposure period (maximum one-hour average

and maximum population-weighted annual exposure).

For the maximum one-hour average exposure, the cumulative toxicological endpoints of

concern are eye irritation and respiratory irritation. Table 8 displays the individual HQs for each

chemical where eye irritation is a primary toxicological endpoint. PAN, ozone, and nitrogen

dioxide are the major pollutants that cause the eye irritant effects. Under the cumulative impact

methodology, sub-threshold pollutants such as acetaldehyde and formaldehyde may also

participate by exacerbating the eye irritation primarily due to PAN, ozone, and nitrogen dioxide.

For acute respiratory irritation, ozone and nitrogen dioxide are the major pollutants of

concern. Acetaldehyde may also exacerbate the respiratory irritation caused by ozone and

nitrogen dioxide (Table 9). The ethanol and MTBE contribution to both eye and respiratory

irritation tend to be so small that these pollutants are not likely to have a significant impact on

these toxicological endpoints.

The primary pollutants involved in chronic respiratory irritation are formaldehyde and PM10,

both of which are individually above the threshold for this toxicological endpoint (Table 10) and

may result in chronic respiratory effects at the maximum exposure level. A limitation in using

the cumulative impact approach for pollutants that cause either acute or chronic respiratory

irritation is that their primary site of action within the respiratory system may differ. For

example, formaldehyde is known to produce nasal and upper respiratory irritation while PM10

produces inflammation principally in the lower airways. Therefore, the cumulative impacts for

these two pollutants may be less than additive.
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Table 8. Maximum Acute Hazard Quotients (HQ) and Cumulative Acute Hazard Indices (HI) for Eye Irritation

for Each of the Five Fuel Scenarios

Chemical 1997

MTBE

2003

MTBE

2003

Et2%

2003

Et3.5%

2003

NonOxy

Upper 0.3 0.3 0.3 0.3 0.3 Acetaldehyde

Lower 0.2 0.2 0.2 0.2 0.2

Upper 0.002 0.002 0.003 0.003 0.002 Ethanol

Lower 0.001 0.001 0.002 0.003 0.001

Upper 0.5 0.5 0.5 0.5 0.5 Formaldehyde

Lower 0.3 0.3 0.3 0.3 0.3

Upper 0.01 0.007 0 0 0 MTBE

Lower 0.003 0.002 0 0 0

Upper 5.5 5.3 5.2 5.3 5.1 PAN

Lower 2.7 2.7 2.6 2.7 2.5

Nitrogen dioxide Best 1.0 0.9 0.9 0.9 0.9

Ozone Best 2.7 2.6 2.6 2.5 2.6

Cumulative HI Upper 10.0 9.6 9.5 9.5 9.4

Lower 6.9 6.7 6.6 6.6 6.5

Table 9. Maximum Acute Hazard Quotients (HQ) and Cumulative Acute Hazard Indices (HI) for Respiratory

Irritation for Each of the Five Fuel Scenarios

Chemical 1997

MTBE

2003

MTBE

2003

Et2%

2003

Et3.5%

2003

NonOxy

Upper 0.3 0.3 0.3 0.3 0.3 Acetaldehyde

Lower 0.2 0.2 0.2 0.2 0.2

Upper 0.002 0.002 0.003 0.003 0.002 Ethanol

Lower 0.001 0.001 0.002 0.003 0.001

Upper 0.01 0.007 0 0 0 MTBE

Lower 0.003 0.002 0 0 0

Nitrogen dioxide Best 1.0 0.9 0.9 0.9 0.9

Ozone Best 2.7 2.6 2.6 2.5 2.6

Cumulative HI Upper 4.0 3.8 3.8 3.7 3.8

Lower 3.9 3.7 3.7 3.6 3.7
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Table 10. Maximum Chronic Hazard Quotients (HQ) and Cumulative Chronic Hazard Indices (HI) for

Respiratory Irritation for Each of the Five Fuel Scenarios

Chemical 1997

MTBE

2003

MTBE

2003

Et2%

2003

Et3.5%

2003

NonOxy

Upper 0.4 0.3 0.3 0.4 0.3 Acetaldehyde

Lower 0.4 0.3 0.3 0.3 0.3

Best 0.0001 0.0001 0.0001 0.0002 0.0001 Ethanol

Upper 2.4 2.1 2.1 2.1 2.0 Formaldehyde

Lower 2.4 2.1 2.0 2.0 2.0

Nitrogen dioxide Best 0.8 0.8 0.8 0.8 0.8

PM10 Best 1.9 1.9 1.9 1.9 1.9

Cumulative HI Upper 5.5 5.1 5.1 5.2 5.0

Lower 5.5 5.1 5.0 5.0 5.0

Other limitations may exist for determining the cumulative toxicological impacts of airborne

pollutants. Combining HIs may underestimate the effect in the cases where interactions on a

given target organ are synergistic, or overestimate the effect in the cases in which interactions are

not additive or are antagonistic.

A limitation concerning the acute HIs is that the peak one-hour airborne concentrations for

each of the chemicals may not have occurred in the same hour. However, given that the onehour maximum average is a worst case scenario for an episodic event, it is appropriate to assume

for the purposes of the cumulative impact analysis that peak one-hour concentrations occur

during the same time period.

The modeling conducted by CARB to evaluate the differences in air quality impacts from

using the various fuel formulations provided the concentrations in air that we have used in this

analysis. The concentrations for acute exposures (e.g., 1, 8, 24 hour averages) reflect a scenario

with relatively adverse meteorological conditions. In addition, the model is based on the South

Coast Airshed, in which pollutant concentrations from vehicular and other sources are typically

somewhat higher than in some other areas of the State of California. Therefore, the absolute

values of the annual average concentrations may not reflect an average in other parts of the State.

There is more confidence assigned to the relative values of the concentrations representing the

various fuel usage scenarios.

Overall, OEHHA finds that the modest reduction in HIs for the 2003 fuel scenarios compared

to the 1997 fuel scenario is encouraging. The cumulative HIs imply that at times some

individuals may experience eye and respiratory irritation. However, given the above limitations

in the cumulative impact methodology, as well as uncertainties in modeled exposure and

toxicological risk methodology, the very minor differences in the predicted cumulative

noncancer impacts among the year 2003 fuel scenarios are not significant enough to warrant a

recommendation for any one fuel based solely on airborne exposure to eye and respiratory

irritants.
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6.5. Health Impacts of Drinking Water Contamination by

Gasoline Components

Health protective concentrations for drinking water for various components of gasoline are

shown in Table 3.

The compounds of greatest concern from the point of view of potential low-level

contamination of drinking water are benzene (a known human carcinogen) and MTBE. MTBE

is a suspected carcinogen, and also has highly objectionable taste and odor which render drinking

water unpalatable even at very low concentrations. Its breakdown product, TBA, is also a

suspected carcinogen and has similarly objectionable organoleptic (i.e. noxious) properties.

Other compounds for which some adverse health effects might be anticipated are toluene,

xylene, formaldehyde, and various aliphatic hydrocarbons. These are not considered

carcinogenic by the oral route, but higher concentrations are toxic, and some may also adversely

effect taste and odor. Ethanol and its oxidation products such as acetaldehyde are toxic only at

very high levels and are also very rapidly biodegraded, so in general these are not expected to

present major long-term contamination problems.

Contamination of ground and surface waters by gasoline components, as a result of leakage,

spills and transportation accidents is an established fact, and likely to continue in spite of efforts

to prevent such occurrences. However, the organizations responsible for providing public

drinking water supplies have monitoring and control measures in place for contaminants with

potentially adverse impacts on public health. OEHHA has been advised by the State Water

Resources Control Board (SWRCB) that it is the policy of the California Department of Health

Services’ (DHS) Drinking Water Program to avoid contamination of any public water supply by

gasoline components in excess of the health protective levels. This may include closing down

wells or surface water sources that show signs of contamination. They also monitor the

movement of known plumes from gasoline spills and leaks. These measures are intended by the

SWRCB to ensure that public drinking water supplies remain free of contamination by gasoline

components, and thus prevent adverse public health consequences for consumers of the public

drinking water supply. This would be the case either with continued use of MTBE, or with its

replacement by ethanol or non-oxygenated gasoline. There may be extensive economic

consequences and resource availability problems if well closures are widespread. These

consequences, and their differential impact in scenarios with use of different fuel compositions,

are the subject of a separate report by SWRCB (Volume 4).

There is a concern for public health impacts of different fuel formulations for those using

private wells or other sources of drinking water not subject to the monitoring and regulatory

oversight of the DHS Drinking Water Program. OEHHA has so far been unable to determine the

number and location of such sources that may be threatened by gasoline spills, or the number of

people using them as their drinking water sources. There appears also to be little quantitative

information on the differential impact of alternative fuel formulations on contamination levels in

affected wells. It has not therefore been possible to provide a quantitative risk assessment for

this situation. Qualitatively, it would appear that MTBE is already a problem for groundwater

users, and its removal would be an unqualified benefit. Direct effects of ethanol would appear to

be minimal even in cases of severe contamination, although the adverse consequences of

contamination by the hydrocarbon fraction of the gasoline would remain. Research is currently
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being undertaken to determine whether any secondary effects of ethanol, such as enhancement of

migration through soil, or acceleration or inhibition of biodegradation, would alter the

concentrations of compounds of concern (such as benzene) in impacted wells.

No investigations of the systemic effects of oral exposure to very low levels of ethanol, such

as might be anticipated if groundwater contamination were to occur, were identified in the

literature. It is known that ethanol is rapidly biodegraded, and expected exposures are low. This

issue is the subject of more detailed investigations currently being undertaken for the SWRCB.

Since the results of this investigation are not yet available, the CalTox model was used as a

preliminary approach for a typical situation of contaminated soil, with literature values for

ethanol degradation, etc. Starting with 10,000 ppm in soil and 5,000 ppm in the vadose zone, the

predicted values in ground water and tap water at one year were 2.3 × 10-6 and 1.9 × 10-6 ppm,

respectively. Human exposure was 8% by inhalation, 91% by oral and 1% by dermal routes. As

an extreme worst-case scenario, the values for half-lives of ethanol in soil and water were

increased by an order of magnitude and the exposure time shortened to begin at 50 days instead

of one year. In this case, the water concentrations were 0.24 and 0.20 ppm, respectively. Human

exposure via tap water was assumed to be 10% by inhalation, 89% by oral, and 1% by dermal

routes. These concentrations are well below the health protective concentrations developed in

Appendix A and are also well below concentrations normally found in foods.

Overall, these findings indicate that ethanol contamination of the water due to use of ethanol

in gasoline should present very minimal toxic and carcinogenic risk and no objectionable taste or

smell problems for public drinking water.

6.6. Uncertainties and Data Gaps

6.6.1. Uncertainties in Dose-Response Assessment

Risk assessment involves a number of assumptions. Due to data limitations, it is not possible

to ascertain all the uncertainties inherent in any cancer potency or unit risk factor. As a result of

a number of uncertainties (e.g., in the cases where human data were inadequate for risk

assessment, applicability of animal data to humans, variability in response in the general

population, presence of susceptible subpopulations, etc.), the unit risk factor represents generally

the 95 percent upper confidence limit of the slope of the dose-response curve. As such it may be

considered a high-end estimate of the risks. The RELs for non-carcinogenic effects also have

similar associated uncertainties. In developing RELs, uncertainty factors are applied to animal

or human data to arrive at a concentration of the chemical in question that we are reasonably

confident will not be associated with adverse health effects from long-term exposure. Thus,

there is a built in margin for health-protection in the REL. These types of uncertainties are not

readily quantifiable and in some instances, not quantifiable at all.

Most of the health values (unit risk factors, cancer potency factors, reference exposure levels)

used in the evaluation were peer-reviewed numbers currently in use in a number of regulatory

and advisory programs. In several instances, there was no available regulatory number. For

example, there is no acute REL for butadiene and OEHHA has provided an interim value for a

one-hour averaging time. Likewise, there is no regulatory value for ethanol in either air or water.
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OEHHA has evaluated secondary literature and the key primary studies to develop interim

values for use in this assessment as reference exposure levels in air and water.

A similar situation exists for other important chemicals of interest. The atmospheric

transformation product, peroxyacetyl nitrate or PAN, is an irritant gas due to its oxidant

properties. Despite the fact that PAN was identified as an irritating component of smog decades

ago, no peer-reviewed regulatory numbers exist to use in a health effects assessment. We

developed interim health protective concentrations for PAN for one hour and annual averaging

times. A related compound, peroxypropionyl nitrate or PPN, is also an irritant gas formed via

atmospheric reactions. However, we could not locate adequate toxicity information on this

chemical and so have not included formation of PPN in this evaluation.

Other chemicals of interest lack key toxicity data. Nonoxygenate formulas of gasoline will

likely have increased levels of alkylates relative to fuels with an oxygenate, including

2-methylpentane, 3-methylpentane, methylcyclopentane, 2,3-dimethylpentane, 2,4-dimethylpentane, 2,2,4-trimethylpentane, 2,3,4-trimethylpentane, 2-methylhexane, and 3-methylhexane.

These branched chain hydrocarbons function much the same as an oxygenate by increasing the

efficiency of combustion. There are almost no toxicological data on these compounds. We are

therefore unable to estimate potential public health risks from increasing the concentrations of

these motor fuel components in the non-oxygenate fuels. However, the concentrations of these

compounds modeled for the South Coast Air Basin for existing fuel speciation profiles are in the

low parts per billion range as an annual average and in the tens of ppb range as one-hour peaks.

Thus the alkylates would need to be fairly potent toxicants (e.g., be about equivalent to the

cancer potency of benzene, have much greater acute noncancer toxic potential than benzene, and

have greater chronic toxic potential than benzene) in order for these concentrations to be of

concern. Our inability to estimate public health impacts of alkylates due to the almost complete

lack of toxicological data is an uncertainty in this evaluation.

Finally, this evaluation focused on the key differences resulting from use of four different

fuels. We used available evidence to decide which chemicals are important in assessing the air

quality impacts differences. Although we believe we have focused on the key primary and

secondary pollutants that impact air quality as a result of fuel usage, there is a slight possibility

that the air quality impacts analysis from use of different fuels omitted a significant chemical.

6.6.2. Uncertainties in Exposure Assessment

The concentrations in air modeled by the CARB modeling effort also have inherent

uncertainties. The uncertainty in speciation profiles of the various VOCs in the different fuels

carries into the modeling results. The modeled concentrations are thus subject to uncertainties

due to potential inaccuracies in the species profiles as well as inherent model uncertainties. It is

evident from a comparison of the 1997 and 2003 scenarios with the same MTBE-containing fuel

that the predicted emissions inventory has a substantial dependence on the expected numbers and

types of vehicles. Since the types of vehicles in service and the mileage driven in 2003 are

estimates with a significant level of uncertainty, this uncertainty will carry through to the

exposure estimates for key pollutants. Uncertainty also exists in CARB’s assumption that

reduced air emissions for 2003 are based on a total reduction of overall fuel emissions. As in the

dose-response assessment, uncertainties in modeling may be difficult to quantify. However, they

are likely considerably less than the uncertainties inherent in dose-response assessment. All of
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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the models used by CARB in this exercise have had some validation studies to characterize their

accuracy and guide their improvement. Whatever uncertainty exists in the assessment of

exposure carries into the assessment of risk.

Aside from the air modeling, there are exposure assumptions implicit in some of the health

values used in assessing risk. For instance, the unit risk factors and some of the reference

exposure levels generally contain default assumptions that the average 70 kg person breathes 20

cubic meters per day. A recent analysis of breathing rate distribution conducted by OEHHA

under the Air Toxics Hot Spots program indicates that the value of 20 cubic meters for a 70 kg

person is about the 85th percentile of the distribution of breathing rates. As such it represents an

above-average breathing rate. If the basis of the unit risk factor is a human inhalation study, this

assumption results in a lower estimate of the potency if in fact the subjects were breathing less

air and thus less chemical to produce the observed effect.

There is a very considerable degree of uncertainty over the level of exposure to fuel

components and breakdown products occurring as water contaminants. A primary concern is

exposure via drinking water. (In scenarios involving water as the pathway of exposure, it is

generally assumed that people consume about two liters of water per day. For compounds that

are volatile, they have inhalation exposures equivalent to drinking at least another liter by virtue

of household water use.) We have been unable to perform a quantitative analysis of the risk

from drinking water since estimates of contamination of the sources most likely to be affected,

i.e. private wells, are not available. It is assumed that the DHS Drinking Water Program’s

regulatory and monitoring activities are sufficient to prevent actual delivery of contaminated

water via public distribution systems, in which case there will not be health impacts from this

source. We do not have access to a quantitative evaluation or failure analysis for this

expectation. Some of these uncertainties may be addressed by research currently being

undertaken by the SWRCB.

There may be low-probability scenarios for contamination of water which we have not

evaluated. For example, since ethanol will be transported by truck, train, or barge, the possibility

exists that a transportation accident might contaminate a surface-water drinking water supply.

However, while the aquatic life immediately at the site of the spill might be affected by the

ethanol, it is unlikely that such a scenario would impact public health due to the biodegradability

and relatively low toxicity of ethanol. Similar accidents might also occur with a vessel

transporting already-blended fuel. However, it does not appear useful to focus on that scenario

for the comparative evaluation of ethanol-containing gasoline with other fuels since other

components of fuels of interest (e.g. benzene, toluene, hexane, xylenes) are more toxic and more

slowly degraded in the environment than ethanol and would become water contaminants in a

blended-fuel spill into surface water.

Finally, it is not yet determined which denaturants will be used to denature the ethanol, as

required by law. Initial proposals include the use of naphtha or similar gasoline-like materials,

so these are unlikely to have a substantial effect on the health impacts of the combined fuel.

However, since both the actual composition of such additives and their toxicological properties

are unknown to us at present, we have not evaluated potential health risks of denaturants in the

ethanol used for gasohol.
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7. Research Needs

As noted earlier in this report there are several issues which cannot be addressed, or for

which our assessment is subject to very substantial uncertainties, due to lack of information

which would be required to better define expected risks. Whereas some of the uncertainties are

intrinsic to the process of risk assessment, some could be substantially reduced by further

research. Potential areas for further research relate to both the toxicological properties of

presently identified pollutants and the assessment of exposure to these materials (and perhaps to

others as yet unidentified). These are summarized in Tables 11 and 12.

Table 11. Research Needs for More Complete Understanding of the Potential Health Effects of Ethanol in

Gasoline.

Basic Toxicologic Information Needed:

Alkylates, including but not limited to

2-methyl pentane 2,3-dimethylpentane 2,3,4-trimethylpentane

3-methylpentane 2,4-dimethylpentane 2-methylhexane

methylcyclopentane 2,2,4-trimethylpentane 3-methylhexane

Other compounds:

ethanol (at low concentrations)

isobutene

peroxyacetyl nitrate (PAN)

peroxyproprionyl nitrate (PPN)

Development of Health Assessment Values Needed:

acetaldehyde (acute exposures)

butadiene (acute exposures)

ethanol (acute and chronic exposures)

MTBE (acute exposures)

PAN (acute and chronic exposures)

PPN (acute and chronic exposures)
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

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Table 12. Key Issues to be Resolved in Order to Further Our Understanding of the Potential Health Effects of

Ethanol in Gasoline

Water contamination issues:

what are the gasoline breakdown products?

what is the likelihood of contamination of public / private wells?

what are the impacts of transportation accidents?

what are the impacts of watercraft use?

General risk assessment issues:

what denaturants will be used in the new formulations?

what are the risks posed by, and interactions of, complex mixtures associated with motor fuels?

need to conduct life-cycle analysis to determine overall exposure from production, use and disposal of motor fuels;

this will include air emissions as well as contamination of water and soil

need more information on localized ‘hot spots’

address remaining uncertainties in emissions and atmospheric chemistry

The components of existing and proposed gasoline formulations include several compounds

for which there is relatively little toxicological information available. This applies particularly to

the branched-chain alkanes and alkenes classified as “alkylates”. Whereas these compounds

occur to some extent in all of the fuel formulations considered in this report, they are specifically

increased in the proposed non-oxygenated RFG3 fuel. There appears to be only very limited

acute toxicological information on a few of these compounds, and none at all on many. Further

investigation of those specific chemicals identified as major “alkylate” components of the new

fuels is warranted, to include investigation of both short-term and long-term effects. Studies

need to be performed on specific isomers, rather than on generic fractions such as pentanes,

hexanes, octanes etc., because the toxicological properties of different isomers may differ

substantially. There are some reports on the toxicological properties of generic mixtures,

including previous formulations of unleaded gasoline (U.S. EPA, 1987). While these have

assisted in quantifying the risk from fuels in general, they do not provide sufficient information

on individual components to allow analysis of the differential impact of alternative fuel

formulations.

In spite of the very large literature on the effects of consumption of alcoholic beverages,

there is also a surprising lack of information on the toxicity of ethanol by inhalation, and on the

effects of low level oral ingestion. This may reflect a consensus that ethanol occurs in many

foods and the toxicity of ethanol is not considered a substantial problem under these

circumstances. Nevertheless, it would be preferable to have more complete studies of acute and

chronic effects, performed according to modern experimental design principles. Continued

research on the toxicity of ethanol-containing gasoline also would have merit.

The toxicological information available on the photochemical reaction product PAN is

limited. Although there are data on acute effects, there has been no evaluation for carcinogenic

effects. Some genotoxic effects have been observed, and studies of up to six months duration

identified squamous metaplasia in the respiratory tract of mice. While these latter findings were
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

34

not considered evidence of neoplasia, they do raise the concern for possible carcinogenicity of

this compound, suggesting a more exhaustive investigation using a lifetime bioassay protocol

would be desirable. We were unable to locate any toxicological information on the related

compound PPN. Since both these photochemical reaction products appear to have the potential

for significant health impacts after both acute and chronic exposures, more information on their

effects would be highly desirable.

Actual exposures to chemicals associated with fuels most commonly occur as exposures to

complex chemical mixtures, rather than to isolated chemicals; thus, it is important that the health

effects of interactions between individual components of these mixtures be characterized, in

addition to the health effects of the individual components. There are presently large gaps in our

knowledge of the health effects of exposures to complex mixtures associated with gasoline, as

well as the health effects associated with some individual compounds. There is a need to

conduct original research and to further develop and evaluate existing epidemiological data on

the human health effects from complex mixtures associated with fuel components.

Additional research is also needed to address uncertainties in the exposure assessment.

While the emissions and atmospheric chemistry have already been the subjects of extensive

study, and a sophisticated model is available, significant uncertainties remain. It is important

that monitoring of the actual atmospheric pollutant levels be continued, to observe the outcome

of changes in vehicle type and usage and fuel composition, and thereby to confirm the accuracy

of the model predictions.

It is also evident that at present our knowledge of the possible exposures via drinking water is

limited. This needs to be augmented in several respects. An analysis of the likelihood of

contamination of the public drinking water supply, in spite of the regulatory and monitoring

efforts in place to avoid this, should be undertaken. This needs to reflect the number of sources

potentially affected, the frequency of monitoring of these sources, and the size of the potentially

impacted populations. This analysis also needs to provide indications of the possible

concentration ranges and duration of exposures that might arise in the event of a failure of the

control measures. An equally pressing concern is the lack of information of the likelihood and

severity of exposures to gasoline components due to contamination of private wells at risk from

contamination.

Life-cycle analysis integrates the multi-media risks associated with production, use, and

disposal of substances. This is a resource intensive proposition; none the less it should be

attempted for reformulated fuels. Life-cycle analysis would look at such issues as contamination

of the environment from production, transportation, use, dissemination (e.g., at gasoline

stations), and disposal. It is understood that work is at present being undertaken by SWRCB to

address the likelihood of contamination from watercraft engine emissions, leaks, spills, and

transportation accidents. The conclusions of these current efforts are clearly important. In

addition, there is a need to investigate the concentrations of pollutants (gasoline components and

their breakdown products) that might occur in drinking water as a result of such events. While it

may not be possible to predict actual outcomes from likely sources of contamination, it would be

useful to have some information as to the severity of plausible incidents.
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8. Summary / Conclusions

Predicted levels of atmospheric pollutants for different fuel composition scenarios were

provided by the CARB. Fuel compositions represented currently available MTBE-containing

oxygenated fuel, two formulations of ethanol-containing fuel with either 2 or 3.5 percent oxygen

content, and a non-oxygenated fuel formulated to comply with the proposed RFG3 requirements.

These were considered in exposure scenarios based on the predicted emissions inventory for the

year 2003. A scenario of the 1997 emissions inventory and MTBE-containing fuel was used to

calibrate the model against actual measured data for that year.

Health protective concentrations in air and water for compounds of concern in the gasoline

formulations, primary exhaust emissions or transformation products were selected from current

California or United States regulatory standards where these were available. In the absence of

suitable regulatory levels, draft levels currently under development for California programs were

used, or else draft health protective levels were developed for this report using standard

methodology.

The health protective levels for air contaminants were compared to the model predictions for

these compounds provided by CARB, and risk characterizations developed for individual

compound impacts. Risk characterizations of the cumulative impacts of carcinogens and irritant

compounds were also developed.

It appears that there are no substantial differences in the public health impacts of the different

non-MTBE fuel formulations considered in the scenarios for the year 2003. MTBE-containing

fuels still pose a risk to water resources due to the high water solubility coupled with slow

environmental degradation of MTBE. For all of these fuels the concentrations of irritants

(including both air toxics and criteria pollutants) may achieve levels at which the safety margins

for short-term and long-term exposures are reduced. At these levels, adverse health effects are

not necessarily expected, but more sensitive members of the population may be affected. The

2003 scenarios are based on relatively adverse meteorological conditions in a region (the South

Coast Airshed) of California severely impacted by vehicle-generated pollution, so effects in

other parts of the State and under different meteorological conditions will likely be less severe.

Due to the reduction in overall emissions, all the scenarios for year 2003 show a significant

improvement over the predicted averages for 1997. The pattern for airborne carcinogens is

similar in that the overall estimated risks do not differ between fuel formulations, but show some

improvement for 2003 relative to 1997. The absolute values of the risk estimates are not

regarded as reliable indicators of the actual risks faced by the population in the South Coast

region, but are regarded as useful in indicating the relative impacts of the different scenarios.

Due to the lack of quantitative information on possible public exposures as a result of fuelrelated groundwater, surface water or drinking water pollution, it was not possible to provide risk

estimates for public health impacts of water contamination. However, consideration of the

relative toxicity of ethanol, MTBE and their degradation products suggests that the direct effects

of ethanol (if any public exposure were to occur) would be substantially less severe than the

effects of MTBE. Secondary effects, including alterations in distribution and biodegradation of

other fuel components, are currently being evaluated by the SWRCB. They are also examining

the possible impacts of various contamination scenarios, such as spills, leakage, transportation

accidents and the use of gasoline-powered watercraft, on water contamination by fuel
OEHHA REPORT ON EtOH IN GASOLINE – 02/15/00

36

components. Further analysis of the relative effects on water of the different fuel formulations

may be possible once these studies are complete.

Our analysis of the health effects of ethanol in gasoline is dependent on the modeled

concentrations provided by the CARB. As CARB updates their atmospheric concentration

estimates, this report will be updated to reflect any possible new findings and conclusions.

9. References

OEHHA (1997). Public Health Goal for Xylenes in Drinking Water. Office of Environmental

Health Hazard Assessment.

OEHHA (1999a). Air Toxics Hot Spots Program Risk Assessment Guidelines. Part I. The

Determination of Acute Reference Exposure Levels for Airborne Toxicants. Prepared by the Air

Toxicology and Epidemiology Section, Office of Environmental Health Hazard Assessment.

March 1999.

OEHHA (1999b). Air Toxics Hot Spots Program Risk Assessment Guidelines. Part II. Technical

Support Document for Describing Available Cancer Potency Factors. Prepared by the Air

Toxicology and Epidemiology Section, Office of Environmental Health Hazard Assessment,

April 1999.

OEHHA (1999c). Public Health Goal for Benzene in Drinking Water. Office of Environmental

Health Hazard Assessment.

OEHHA (1999d). Public Health Goal for Methyl Tertiary-Butyl Ether (MTBE). March. Office

of Environmental Health Hazard Assessment.

OEHHA (1999e). Public Health Goal for Toluene in Drinking Water. Office of Environmental

Health Hazard Assessment.

U.S. EPA (1987). Evaluation of the carcinogenicity of unleaded gasoline. Carcinogen

Assessment Group, Office of Health and Environmental Assessment, Office of Research and

Development. EPA/600/6-87/001. Washington DC, April 1987.

U.S. EPA (1999). Benzene. Carcinogenicity Assessment for Lifetime Exposure. Integrated Risk

Information System, Washington, D.C. U.S. Environmental Protection Agency. Last Revised;

10/16/98.