Chapter 2

Risk-Based 

Strategy

2012 PM2.5 Plan

SJVUAPCD
San Joaquin Valley Unified Air Pollution Control District December 20, 2012

Chapter 2: Risk-Based Strategy

2012 PM2.5 Plan 

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Chapter 2: Risk-Based Strategy

2.1 WHAT IS THE RISK-BASED STRATEGY?

The U.S. Environmental Protection Agency’s (EPA) National Ambient Air Quality 

Standards (NAAQS) are the primary driving force for new emissions controls that result 

in air quality improvements and health benefits to Valley residents. In the conventional

planning process for attaining these standards, success in protecting public health is 

defined by whether the standards are met at all air monitors. In effect, the reduction in 

PM2.5 mass, which shows progress toward attainment of the standard, serves as the 

surrogate for population exposure and risk. 

NAAQS are indeed health-based, and attaining these standards will result in clear and 

significant health benefits. However, NAAQS, as currently established, are essentially 

mass-based standards. In the case of PM2.5, the current standards do not account for 

particle size distribution, chemical species composition, surface area, and other factors 

of health risk. There is inherent complexity in documenting the health risks associated 

with exposure to particles (which have a wide range of characteristics) as compared to 

pollutants like ozone (which has more consistency between molecules).

In contrast, recent health-science research has substantially deepened our knowledge 

of air pollutant health risk beyond the current Clean Air Act (CAA) framework and EPA 

standards. There is a growing recognition within the scientific community that the 

NAAQS alone can be incomplete measures of public exposure to air pollution. Thus, 

while the CAA’s NAAQS and state implementation plan (SIP) process is motivated by 

public health, the process alone does not fully address public health impacts of ambient 

air pollution. To fully address potential public health benefits, an attainment strategy 

can use a more comprehensive, multidimensional population exposure assessment 

approach that goes beyond ambient mass measurements.

1

EPA policy directly acknowledges the importance of a Risk-based Strategy to maximize 

public health benefits within a region’s efforts to attain the National Ambient Air Quality 

Standards (NAAQS). EPA’s March, 2012, PM2.5 implementation guidance memo 

states, “...it is likely that SIPs for the 2006 24-hour PM2.5 NAAQS may need to include 

greater emphasis on reducing emissions from local sources [emphasis added] as 

compared to plans to attain the 1997 PM2.5 NAAQS.”2 EPA’s memo further encourages 

that states consider evidence from published literature indicating that reductions of 

direct PM2.5 have a greater health benefit per ton than reductions of other criteria 

 

1

Lippman, M. (2012, April 16). Presentation: Results from National Particle Component Toxicity (NPACT) Program 

and NYU: Toxicology Findings, Integration, and implications. Presented at the Annual Meeting of the Health Effects 

Institute (HEI) in Chicago, IL, April 15–17, 2012. Presentation retrieved from 

http://www.healtheffects.org/Slides/AnnConf2012/Lippmann-MonPM.pdf

2 U.S. Environmental Protection Agency (2012, March 2). Memorandum from the Office of Air Quality Planning and 

Standards: Implementation Guidance for the 2006 24-Hour Fine Particle (PM2.5) National Ambient Air Quality 

Standards (NAAQS). Retrieved from http://www.epa.gov/ttn/naaqs/pm/pdfs/20120302_implement_guidance_24-

hr_pm2.5_naaqs.pdf
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pollutants, such as SO2 and NOx,3and that providing methods local air quality plans 

can use to maximize health benefits and minimize risk inequality.4

In September 2010, the District Governing Board adopted a research-driven Risk-based 

Strategy (RBS) designed to maximize public health improvements resulting from the 

District’s attainment strategies and related initiatives. The overall goal of the RBS is to 

minimize cumulative population exposure to air pollution and corresponding health risk 

in the region. This risk reduction goal is being pursued through the integration of

emerging scientific knowledge into the District’s control strategies, incentive programs, 

public communication, and enforcement actions. 

The District is integrating the RBS into the development of the 2012 PM2.5 Plan. The 

purpose of this chapter is to document the scientific foundation for the RBS and how it is

being applied to the District’s PM2.5 SIP. This chapter includes the following elements: 

 The key aspects of particulate pollution that shape human exposure and risk 

from PM2.5, along with a discussion of how the RBS is reflected in existing 

District programs; 

 Further details about key health risk elements of PM2.5 particles and exposure; 

and 

 An outline of how these risk elements are used to characterize the associated 

risk when evaluating sources of PM2.5 and related control or incentive options in 

subsequent chapters.

2.2 BACKGROUND FOR THE RISK-BASED STRATEGY 

As a response to mounting epidemiological evidence that PM2.5 was more harmful than 

PM10, EPA established a PM2.5 NAAQS in 1997 to accompany the previously 

established PM10 NAAQS. PM10 occurs at larger mass concentrations than PM2.5, so 

the shift to PM2.5 somewhat conflicted with the time-tested toxicological precept of “the 

dose (mass) makes the poison.” Particulate inhalation studies found that the smaller 

PM2.5 particles penetrate more deeply into the lungs, where particles more effectively 

avoid immune system defenses. Toxicological analyses of PM2.5 identified chemical 

species that acted differentially to promote respiratory and cardiovascular inflammation. 

While it was unclear at that time which PM2.5 chemicals were the most harmful, the 

scientific consensus was that the health risks stemmed from the chemicals rather than 

the particles themselves. 

In the 15 years since the first PM2.5 NAAQS was established, scientists have 

conducted many studies that have identified which chemical species of PM2.5 are most 

 

3

Fann, N., Fulcher, C.M., & Hubbell, B.J. (2009). The Influence of Location, Source, and Emission Type in Estimates 

of the Human Health Benefits of Reducing a Ton of Air Pollution. Air Quality, Atmosphere & Health, 2(3), 169–176. 

doi: 10.1007/s11869-009-0044-0

4

Fann, N., Roman, H.A., Fulcher, C.M., Gentile, M.A., Hubbell, B.J., Wesson, K., & Levy, J.I. (2011). Maximizing 

Health Benefits and Minimizing Inequality: Incorporating Local-Scale Data in the Design and Evaluation of Air Quality 

Policies. Risk Analysis, 31(6), 908–922. doi: 10.1111/j.1539-6924.2011.01629.x
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harmful and have pinpointed their sources.

5

 Health researchers have also documented

the negative cardiovascular and immune system effects of ultrafine particles, or 

particles that are 0.1 microns or smaller (PM 0.1), based on these particles’ ability to 

penetrate the alveolar region of the lungs and deliver chemicals into the bloodstream. 

This smaller-is-more-dangerous phenomenon parallels the previous discovery regarding

the higher toxicity of PM2.5 particles compared to larger and heavier PM10 particles. In 

each case, the dose-makes-the-poison assumption governing the NAAQS for carbon 

monoxide, lead, ozone, and the other criteria pollutants does not apply to particulates. 

Addressing the complexity of health risks posed by particulate pollution has been a 

motivating factor in the development and application of the RBS. Rather than ignore 

this growing body of scientific knowledge in the development of this SIP, the District’s 

RBS seeks to embrace it to the extent possible within the current CAA to maximize

public health benefits. In practice, this knowledge provides the District with the 

necessary scientific foundation for justifying and prioritizing the pollution control 

measures that are necessary for demonstrating attainment in this plan. The outcome is 

a stronger, more health-protective plan that reflects the current trajectory of scientific 

knowledge toward a more complete understanding of population risk from PM2.5 

particles. 

The NAAQS-SIP process and the RBS are complimentary strategies, not an either-or 

scenario. The RBS should not be interpreted as a zero-sum tradeoff that emphasizes 

controls on certain forms and sources of high-risk PM2.5 while ignoring others. The 

current mass-based indicator (micrograms per cubic meter of air) will continue to serve 

as the final yardstick for PM2.5 attainment and as a surrogate for achieving significant 

health benefits. As required under the CAA, the District is committed to attaining the 

2006 PM2.5 standard as expeditiously as possible, and the District will not ignore

sources of PM2.5 under its jurisdiction that could contribute to the Valley’s attainment of 

the PM2.5 NAAQS. 

A number of the District’s programs have been influenced by the underlying principles

and goals of the Risk-based Strategy and provide a model of the success and added

potential benefits possible under this strategy.

 District Rule 4901 (Wood Burning Fireplaces and Wood Burning Heaters) 

and the District’s corresponding Check-Before-You-Burn program have

both been reducing harmful species of PM2.5 where and when those reductions 

are most needed—in impacted urbanized areas when the local weather is 

forecast to hamper PM dispersion. By decreasing emissions from residential 

wood burning, Rule 4901 decreases directly emitted PM2.5, as well as carbon 

monoxide, formaldehyde, sulfur dioxide, irritant gases, and known and suspected 

carcinogens, such as polycyclic aromatic hydrocarbons (PAH). In 2008, the 

Central Valley Health Policy Institute found that District wood burning 

curtailments on days with high PM concentrations reduced annual PM exposure 

 

5 U.S. Environmental Protection Agency [EPA]. (2009). Integrated Science Assessment for Particulate Matter: Final 

Report. Washington, D.C.: EPA/600/R-08/139F. Available at 

http://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=216546
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by about 13% in Bakersfield and Fresno, resulting in an estimated 59 to 121

avoided cases of annual premature mortality.

6

Even though the 2008 PM2.5 Plan was developed per EPA requirements for the 

1997 PM2.5 standard (with a 24-hour standard of 65 μg/m3), the 2008 plan

included a commitment to amend Rule 4901 in 2009 (with implementation in 

2010) to align the wood-burning curtailment threshold with the newer 2006 

PM2.5 standard (with a 24-hour standard of 35 μg/m3). Then, based on research 

reiterating the effectiveness of Rule 4901 in protecting public health, as well as 

public support for a stronger rule, the District amended and implemented Rule 

4901 in 2008—one year ahead of the scheduled rule development and two years 

ahead of scheduled implementation. The amended rule also set the curtailment 

level lower than initially planned (to 30 μg/m3) to provide an extra margin of 

safety and to address air quality forecast uncertainties. 

The significant increase in the number of curtailment days resulting from the 

lower threshold has resulted in a parallel reduction in nighttime neighborhood 

exposure to PM 0.1, including exposure that has been shown to occur as a result 

of indoor infiltration. This aspect of Rule 4901, i.e. reducing the frequency of 

elevated exposure to PM0.1 that induces immune system sensitization and 

cardiovascular inflammation, has been carried forward into the Risk-based 

Strategy. The District’s prioritization of Rule 4901 is one of the best examples of 

a District policy aimed at maximizing public health benefits based on a rigorous 

assessment of population exposure and risk.

 District grant programs reach beyond the current CAA NAAQS-SIP process to 

reduce emissions in advance of or beyond regulations. For example, through the 

District’s popular Clean-Green-Yard-Machine grant program, the District has 

replaced over 2,000 high-polluting gas-powered lawn mowers with clean electric 

mowers, thus decreasing the urban, localized health risks associated with the 

use of gas-powered equipment. As described in Appendix C of this plan, the 

District is now expanding its lawn care emissions reductions programs to the 

commercial sector. In conjunction, District-funded field measurements of PM 0.1 

by UCSF-Fresno found very high concentrations in and around lawn care 

activities, indicating a very high intake fraction for lawn care workers and 

concomitant cardiovascular risk.

 The District’s information and educational programs, such as the RealTime Air Quality Advisory Network (RAAN), also contribute to the Risk-based 

Strategy. RAAN uses real-time data from air monitoring stations throughout the 

Valley to provide hour-by-hour air quality updates to schools and other 

subscribers. Subscribers can use this information to make informed decisions 

and plan outdoor activities for times with the best air quality, reducing potential 

 

6

Lighthall, D., Nunes, D., & Tyner, T.R. (2009). Environmental Health Evaluation of Rule 4901: Domestic Wood 

Burning. Fresno, CA: Central Valley Health Policy Institute for the San Joaquin Valley Air Pollution Control District. 

Retrieved from http://www.fresnostate.edu/chhs/cvhpi/documents/wood-burning-report.pdf
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air quality health risks. Reflecting the latest science on PM2.5 exposure risk for 

sensitive individuals, ambient concentrations of PM2.5 that are used to trigger 

RAAN health risk warnings are more health protective than those used in the 

EPA’s Air Quality Index.

 The District tracks and sponsors health research. The District has sponsored 

several Valley-based health research projects in recent years. In 2010–2011, the 

District sponsored a first-of-its-kind epidemiological investigation of health effects 

of air pollution in Modesto, Fresno, and Bakersfield.7 The study found that high 

PM and ozone concentrations clearly correlate to increased hospital and ER 

admission rates, especially for those 19 and younger. During 2011 and 2012, 

the District is sponsoring a follow-up epidemiological study to examine which of 

the chemicals found in Valley PM2.5 are most highly correlated with elevated ER 

and hospital admission rates. The District is also sponsoring a pilot study of PM 

0.1 in Fresno, partnering with UCSF-Fresno, to investigate the quantity and 

spatial distribution of PM 0.1 plumes from motor vehicles, lawn care equipment, 

wood burning, and restaurants. The District will continue to seek out and fund 

research opportunities that further the understanding of PM2.5 and ozone 

impacts on public health.

 

2.3 HOW IS THE RISK-BASED STRATEGY BEING INCORPORATED INTO THIS

PLAN?

Though there are several existing District programs that readily fit into this strategy, this 

2012 PM2.5 Plan is the District’s first formal effort to synthesize research, populationexposure analysis, and comprehensive emissions reductions efforts into a cohesive 

Risk-based Strategy. This is also the District’s first opportunity to demonstrate how the 

RBS fits within and effectively supplements EPA’s current CAA framework.

The District is integrating the RBS into various aspects of the 2012 PM2.5 Plan. The

District expects to incorporate the RBS into this plan with the following:

 Information regarding health effects of PM2.5: Chapters 1 and 2 include 

detailed discussions regarding the different types of PM2.5 and their associated 

health effects. 

 Ambient data analysis: In addition to evaluating PM2.5 mass trends per CAA 

and EPA guidelines, Chapter 3 and Appendix A discuss PM2.5 species-based

trends. This species analysis, when considered with health research, will 

highlight which PM2.5 and PM2.5 precursor sources might be prioritized under 

the RBS. The District is also evaluating the timing of higher PM2.5 

 

7 Capitman, J.A., & Tyner, T.R. (2011). The Impacts of Short-Term Changes in Air Quality on Emergency Room and 

Hospital Use in California's San Joaquin Valley. Fresno, CA: Central Valley Health Policy Institute for the San Joaquin 

Valley Air Pollution Control District. Retrieved from http://www.fresnostate.edu/chhs/cvhpi/publications/index.html
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concentrations to see if there are certain times of the day or times of the year 

when PM2.5 reductions might have more public health benefits. 

 Health Research: The RBS is driven by strong science and research, and the 

District will continue to evaluate existing research and assist in promoting new 

research relevant to the Valley.

 Analysis of health benefits under the attainment strategy: Building on 

regional SIP modeling provided by ARB, the District used EPA’s BenMAP benefit 

estimation model to estimate the health benefits in the Valley resulting from the 

District’s attainment strategy. (See section 2.5 and Appendix E for additional 

details)

 Source-by-source assessment: The District is conducting a thorough analysis 

of all potential opportunities to reduce emissions of directly emitted PM2.5 and 

significant PM2.5 precursors in the Valley. The qualitative exposure assessment 

described below will be used to assist in evaluating the potential health benefit of 

reducing emissions from these various sources. This more comprehensive 

assessment will help establish the strongest scientific justification for new source 

control strategies and incentive program investments.

 Control measure/strategy prioritization: Based on the above source-by-source 

assessment, and other evaluation being conducted as part of developing this 

plan, priority will be given to regulatory control measures, incentive programs, 

technology advancement efforts, policy initiatives, and other strategies that 

maximize public health. 

2.4 FIVE-FACTOR EXPOSURE ASSESSMENT METHODOLOGY

To qualitatively evaluate the potential risk reduction benefits from various sources, this 

plan will employ a scientifically based exposure characterization methodology that 

draws on the latest scientific understanding about health risk from PM2.5 exposure. 

The District will use a five-factor exposure assessment methodology under the RBS:

1. Relevance to attainment

2. Toxicity of chemical species 

3. Particle size and deposition 

4. Proximity to PM 0.1

5. Population intake fraction 

The qualitative exposure assessment employed in this SIP is different than a formal risk 

assessment. Risk assessment requires the quantification of key elements relating to 

emission levels, particle or chemical toxicity, dose-response relationships, and total 

population exposure. The primary drawback for formal risk assessment models in a SIP 

context is pervasive empirical uncertainty regarding the values of the different elements 
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listed above. Even if the chemical composition, geographic pattern and volume, and 

spatial distribution of emissions from a given source are known, it is very difficult to 

isolate and quantify the regional health impacts of emissions from that source because 

many other sources are also contributing to PM2.5 exposure. In addition, PM2.5 

aerosols undergo photochemical aging over time and space, often resulting in new 

secondary organic and inorganic species generated by variable regional source loads

and meteorological conditions. Despite these limitations, it is possible to use a simple 

but robust exposure characterization tool for making important qualitative and 

categorical distinctions regarding the relative contribution and associated of a given 

source to population exposure. 

2.4.1 Relevance to Attainment

An important element of the RBS is the relevance of the emissions reductions to the 

Valley’s attainment of EPA’s health-based standards. This portion of the analysis will 

consider emissions type (such as PM2.5, NOx, or SOx), seasonality of the emissions 

(since PM2.5 exceedance days occur during the winter months), and the percent

contribution of that source’s emissions relative to the Valley’s total emissions inventory. 

For example, NOx is the limiting factor for ammonium nitrate and therefore reductions of 

NOx emissions in the Valley will provide a greater impact to achieving attainment than 

reductions of ammonia emissions. 

2.4.2 Toxicity of Chemical Species

PM2.5 particles vary in their toxicity depending on their chemical composition. PM2.5 

particles are characterized by a widely diverse combination of chemicals depending on 

unique regional combinations of meteorology, topography, and pollution sources. In 

addition to experimental and clinical research that has identified these toxicity 

differences, epidemiological studies have found regional differences in health impacts 

despite comparable regional PM2.5 mass exposure.

8

 Beyond the intrinsic toxicity of 

individual chemicals, the unique combinations of chemicals generated by some sources 

can actually magnify health risk above and beyond what their mass concentrations 

would suggest.

9

Many emissions sources evaluated in this plan are sources of direct (primary) PM2.5 

emissions characterized by a unique combination of chemical species. Other sources 

emit chemical species such as ammonia and nitrogen oxides (NOx), precursors that 

contribute to the formation of secondary PM2.5 species. The PM2.5 chemical species 

categories adopted in the exposure characterization model include elemental carbon 

(carbon black), organic carbon compounds (OC), metals (elements), ammonium nitrate, 

 

8

Bell, M.L. (2012). Assessment of the Health Impacts of Particulate Matter Characteristics. Research Report 161. 

Boston: MA. Health Effects Institute. Retrieved from http://pubs.healtheffects.org/getfile.php?u=685

9

Kelly, F.J. (2006). Oxidative Stress: Its Role in Air Pollution and Adverse Health Effects. Occupational 

Environmental Medicine, 60, 612–616. Retrieved from http://oem.bmj.com/content/60/8/612.full doi:

doi:10.1136/oem.60.8.612
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ammonium sulfate, and geological (see Appendix A, Section A.4.9). PM2.5 is regularly 

speciated at several Valley monitoring sites (see Chapter 3, Figure 3-7; and Appendix 

A). The following discussion provides an overview of PM2.5 species and their 

associated health impacts.

Organic carbon (OC): OC species found in PM2.5 aerosol are generated as primary 

organic aerosol (POA), predominantly through the combustion of hydrocarbons. Key 

POA sources include cooking, industrial processes, mobile source exhaust, prescribed 

burning, tire wear, and wood burning.

10

 Secondary organic aerosols (SOA) are formed 

from the oxidation of motor vehicle hydrocarbons, prescribed burning, wood burning, 

solvent use, and industrial processes. 

OC is recognized as one of the most biologically reactive of PM2.5 chemical species 

categories, with ample evidence of high toxicity found in experimental, clinical, and

epidemiological studies. OC, often in combination with metals such as iron, has been 

shown to generate reactive oxygen species (ROS) that drive several different 

mechanisms of pulmonary inflammation, including disruption of normal immune system 

functioning.11 In addition, OC and metals have been shown to indirectly stimulate ROS 

production by macrophages, which are cells responsible for defending the lungs from 

pathogens and aerosols. 

One of the primary OC species categories is polycyclic aromatic hydrocarbons (PAH). 

PAH species fall into two categories: a high molecular weight fraction and a low 

molecular weight fraction. The former is found in diesel exhaust and engine oil and is a 

significant risk factor for lung cancer.

12

 Low molecular weight PAH is found in other 

hydrocarbon combustion particles and serves as a precursor to the formation of an 

important OC species category known as quinones. Formed from atmospheric 

processing of PAH or within the body (in vivo), quinones have been shown to be one of 

the most important drivers of pulmonary oxidative stress, resulting in a host of negative 

spillover effects on immune system functioning.13 Quinone formation via chemical aging 

of PAH occurs during multi-day winter stagnation events in the Valley. A District-funded 

clinical study of asthmatic patients in Fresno found that quinone levels in urine 

 

10 U.S. Environmental Protection Agency [EPA]. (2004, October). Air Quality Criteria for Particulate Matter: Final 

Report. Washington, D.C.: EPA 600/P-99/002aF-bF. Available at 

http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=87903

11 Ayres, J.G., Borm, P., Cassee, F.R., Castranova, V., Donaldson, K., Ghio, A. ... Froines, J. (2008) Evaluating the 

Toxicity of Airborne Particulate Matter and Nanoparticles by Measuring Oxidative Stress Potential—A Workshop 

Report and Consensus Statement. Inhalation Toxicology 20, 75–99. Retrieved from 

http://faculty.unlv.edu/buckb/scanned%20pfd/Ayres%20et%20al%202008.pdf

12 Landvik, N.E., Gorria, M., Arlt, V.M., Asare, N., Solhaug, A., Lagadic-Gossmann, D., & Holme, J.A. (2007). Effects 

of Nitrated-Polycyclic Aromatic Hydrocarbons and Diesel Exhaust Particle Extracts on Cell Signalling Related to 

Apoptosis:Possible Implications for their mutagenic and Carcinogenic Effects. Toxicology, 231, 159–174. 

doi:10.1016/J.tox.2006.12.009

13 Bolton, J., Trush, M.A., Penning, T.M., Dryhurst, G., & Monks, T.J. (2000). Role of Quinones in Toxicology. 

Chemical Research in Toxicology, 13(3), 135–160. doi: 10.1021/tx99
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correlated with sustained (multi-day) high ambient concentrations of PM2.5 and was 

accompanied by decreased lung function.

14

 

Elemental carbon (EC): Elemental carbon is found in combustion-based aerosols 

produced by mobile exhaust (mainly diesel), wood burning, and cooking (especially 

charbroiling). Compared to OC species, there is limited evidence of comparable 

impacts on ROS production, pulmonary inflammation, and immune system disruption. 

For example, EC appears not to be a significant agent for the induction of inflammation 

in macrophage cells, indicating a significantly lower toxicity level relative to OC 

species.

15

 A recent study of PM 0.1-based exposure of EC in mice found modest 

cardiovascular effects. Pulmonary inflammation was noted but only at high doses 

beyond normal ambient concentrations.16 A recent study in Mexico City found an 

association between exposure levels of EC and lung function decrements among 

asthmatic and non-asthmatic children.17 

Characterization of health effects of elemental carbon from human exposure studies is 

complicated by the high correlation between EC, OC, and metals emitted by diesel 

exhaust. Exposure to EC is a PM2.5 risk factor, although there is more evidence to 

date that other chemical species, e.g. metals and OC, found in these particles are the 

primary drivers of negative health effects. 

Metals: A combination of clinical, experimental, and epidemiological studies have 

implicated several of the metals found in PM2.5 with negative respiratory or 

cardiovascular outcomes, sometimes in conjunction with the action of OC species. One 

of the most important is iron because of its ability to catalyze the production of hydrogen 

peroxide, leading to highly reactive hydroxyl radicals (OH). In turn, these highly reactive 

chemicals stimulate the production and action of cytokines by macrophages. Cytokines 

are cell-signaling molecules that are critical to normal functioning of the immune system. 

A recent experimental study examined the impact of iron in silica particles in triggering 

respiratory toxicity.18 Compared to silica particles with no iron, silica particles with iron 

were found to have a significantly greater effect on oxidative stress via hydrogen 

peroxide production with subsequent stimulus of cytokines by macrophages.

 

14 Ikeda, A., Vu, K.K.-T., Lim, D., Tyner, T.R., Krishnan, V.V., & Hasson, A.L. (2012). An Investigation of the Use of 

Urinary Quinones as Environmental Biomarkers for Exposure to Ambient Particle-Borne Pollutants. Science of the 

Total Environment (submitted).

15 Vogel, C.F., Sciullo, E., Wong, P., Kuzmicky, P., Kado, N. & Matsumura, F. (2005). Induction of Proinflammatory 

Cytokines and C-Reactive Protein in Human Macrophage Cell Line U937 Exposed to Air Pollution Particulates.

Environmental Health Perspectives 113(11), 1536–1541.

16 Vesterdal, L.K., Folkmann, J.K., Jacobsen, N.R., Sheykhzade, M., Wallin, H., Loft, S., & Møller, P. (2010).

Pulmonary Exposure to Carbon Black Nanoparticles and Vascular Effects. Particle and Fibre Toxicology 7:33.

Retrieved from http://www.particleandfibretoxicology.com/content/7/1/33 doi: 10.1186/1743-8977-7-33

17 Barraza-Villarreal, A., Escamilla-Nuñez M.C., Hernández-Cadena L., Texcalac-Sangrador. J.L., Sienra-Monge,

J.J., Del Río-Navarro, B., Cortez-Lugo, M., Sly, P.D., & Romieu, I. (2011). Elemental Carbon Exposure and Lung 

Function in Schoolchildren from Mexico City. European Respiratory Journal, 38, 548–552.

18 Premasekharan, G., Nguyen, K., Contreras, J., Ramon, V., Leppert, V.J. & Forman, H.J. (2011). Iron-Mediated 

Lipid Peroxidation and Lipid Raft Disruption in Low-Dose Silica-Induced Macrophage Cytokine Production. Free 

Radical Biology and Medicine, 51(6), 1184–1194. doi: 10.1016/j.freeradbiomed.2011.06.018
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Extensive research relates exposure in metals (particularly nickel and vanadium) in 

PM2.5 to cardiovascular effects. A national epidemiological study recently found that 

communities with higher fractions of nickel, vanadium, and EC in their PM2.5 also had 

higher risk of cardiovascular and respiratory hospitalization.

19

 Specifically, 

cardiovascular hospitalizations were 26% higher in counties with a nickel fraction in the 

75th percentile versus counties with nickel in the 25% percentile. In an investigation of 

the relatively higher association between PM2.5 daily concentrations and daily rates of 

cardiovascular mortality in New York City, the exceptionally high level of nickel and 

vanadium resulting from residual oil fly ash used for heating and as fuel for ships were 

identified as a principle cardiovascular risk factor.

20

 In a related study, rats exposed to 

PM2.5 with high fractions of chromium, iron, and nickel fractions responded with 

significantly reduced heart rate variability and increased heart rates, each being an 

indicator of cardiovascular disruption and risk.21 

In conclusion, metals found in PM2.5 produced from combustion of coal, residual oil, 

diesel fuel, and motor oil are recognized as chemical drivers of cardiovascular and 

respiratory morbidity and mortality. This has led some researchers to conclude that 

regional differences in U.S. cardiovascular mortality that cannot be explained by 

differences in average daily PM2.5 concentrations are likely to be caused by regional 

differences in coal combustion and resultant exposure to metals and OC.

22

Ammonium nitrate: Ammonium nitrate (nitrate) is classified as a secondary inorganic 

species (not directly emitted) primary source of PM2.5, and it does not contain carbon. 

Nitrate is formed by atmospheric reactions between two precursors: ammonia and nitric 

acid. Prior to this reaction, nitric acid generally originates from the chemical processing 

of nitrogen oxides (NOx), largely from fuel combustion under meteorological conditions 

found during Valley winters, particularly during multiday stagnation events. As seen in 

Figure 2-1, nitrate is significant because it can contribute up to 50% or more to PM2.5 

mass during peak days during winter seasons. The percentage contribution of nitrate to 

PM2.5 mass is substantially reduced in summer, with the 2000–2006 Valley average for 

June ranging from 13 to 18%, with mass levels at or below 2 μg/m3.

23

 

 

19 Bell, M.L., Ebisu, K., Peng, R.D., Samet, J.M. & Dominici, F. (2009). Hospital Admissions and Chemical 

Composition of Fine Particle Air Pollution. American Journal of Respiratory Critical Care, 179, 1115–1120. Retrieved 

from http://ajrccm.atsjournals.org/content/179/12/1115.full.pdf+html

20 Lippmann, M., Ito, K., Hwang, J-S., Maciejczyk, P., & Chen, L-C. (2006). Cardiovascular Effects of Nickel in 

Ambient Air. Environmental Health Perspectives, 114(11), 1662–1669. Retrieved from 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1665439/

21 Chen, L.C., & Lippmann, M. (2009). Effects of Metals within Ambient Air Particulate Matter (PM) on Human Health. 

Inhalation Toxicology, 21(1), 1–31. Retrieved from 

http://faculty.unlv.edu/buckb/scanned%20pfd/Chen%20and%20Lippmann%202009.pdf

22 Lippman, M. (2012, April 16). Presentation: Results from National Particle Component Toxicity (NPACT) Program 

and NYU: Toxicology Findings, Integration, and implications. Presented at the Annual Meeting of the Health Effects 

Institute (HEI) in Chicago, IL, April 15–17, 2012. Presentation retrieved from 

http://www.healtheffects.org/Slides/AnnConf2012/Lippmann-MonPM.pdf

23 California Air Resources Board [CARB]. (2011). CARB speciation data: District Staff Analysis of the 2000-2006 

Sampler Data for the Four Speciation Samplers in the San Joaquin Valley. Available at 

http://www.epa.gov/ttn/airs/airsaqs/detaildata/downloadaqsdata.htm
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Figure 2-1 PM2.5 Chemical Composition on Peak Days

A recent cold-season ammonia emissions inventory for the Valley estimated that motor 

vehicles and livestock production each contribute approximately 40% to total seasonal 

ammonia.24 Green waste composting and nitrogen fertilizer emissions from soil are also 

major sources. As temperatures increase, the proportional contribution of livestock to 

the regional inventory increases, peaking at nearly 75% of the total in the hot season. 

The relative toxicity of ammonium nitrate is an important issue given its substantial 

mass contribution to regional PM2.5. The oral toxicity of nitrate is very low, with an

LD50 (dose causing death for 50% of the exposed subjects) reported to be two thirds

that of table salt. This raises the question as to whether other factors intrinsic to 

inhalation could lead to health effects at considerably lower exposure concentrations. 

 

24 Battye, W., Anaja, V.P., & Roelle, P.A. (2003). Evaluation and Improvement of Ammonia Emissions Inventories. 

Atmospheric Environment, 37, 3873–3883.
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As seen in the case of OC species, the most compelling evidence of species toxicity is 

built on a foundation of experimental, clinical, and epidemiological research. In 

particular, epidemiological studies draw their inferences from statistical associations 

between exposure variables and health outcomes only. Uncovering the actual 

mechanisms of harm, therefore, requires further isolation of mechanisms through 

experimental and clinical research. 

In the case of ammonium nitrate, evidence of toxicity is largely limited to epidemiological 

research alone. For example, a recent epidemiological study of traffic air toxics and 

pre-term birth in Los Angeles found statistical associations between nitrate mass, PAH, 

and several other air pollutants and the increased likelihood of pre-term birth.25 The 

authors point to other experimental studies that identified very high oxidative stress 

potential resulting from PAHs, metals, and other OC species collected from Los Angeles 

traffic sources as being the likely mechanism for pre-term birth. They conclude by 

emphasizing the need to further study the links between pre-term birth and PAH 

exposure. 

One experimental study was found that explicitly looked for toxic mechanisms driven by 

ammonium nitrate.26 The study exposed rats to high concentrations of nitrate (70 to 420 

μg/m3) in combination with EC. After exposure, animals were sacrificed and a necropsy 

was performed, followed by a range of tests for pathological impacts between the 

control (non-exposed) and exposed groups. The authors did not find abnormalities that 

could be tied to the experimental exposure to nitrate alone or in combination with EC. 

This absence of experimental evidence for mechanisms of pathology for inhaled 

ammonium nitrate is consistent with its low oral toxicity.

Ammonium sulfate: Ammonium sulfate (sulfate) is also classified as a secondary 

inorganic species. It is formed when sulfuric acid, itself a product of oxidation of sulfur, 

reacts with ammonia. As seen in Figure 2-1, mass concentrations of sulfate are 

significantly lower than for nitrate in the Valley, averaging from 6% to 7% of PM2.5 

mass during winter peaks. Fossil fuel combustion is the primary source of sulfate in the 

Valley, but globally, coal combustion is the primary source. Unlike nitrate, mass 

concentrations of sulfate are not appreciably different in cold and hot seasons.

Research findings regarding the toxicity of sulfate are comparable to that of nitrate. 

Oral toxicity is low and it is approved as a food additive by the US Food and Drug 

Administration and the European Union. One study27 examined the response of 20 

non-smoking subjects to four-hour exposure sessions in chambers containing 500 

μg/m3of sulfate aerosol, a concentration over two orders of magnitude above ambient 

 

25 Wilhelm, M., Ghosh, J.K., Su, J., Cockburn, M., Jerrett, M. & Ritz, B. (2011). Traffic-Related Air Toxics and Preterm 

Birth: A Population-Based Case-Control Study in Los Angeles County, California. Environmental Health 10: 89.

Available at http://www.ehjournal.net/content/10/1/89/ doi: 10.1186/1476-069X-10-89

26 Cassee, F., Arts, J.H., Fokkens, P.H., Spoor, S.M., Boere, A.J., van Bree, L., & Dormans, J.A. (2002). Pulmonary 

Effects of Ultrafine and Fine Ammonium Salts Aerosols in Healthy and Monocrotaline-Treated Rats Following ShortTerm Exposure. Inhalation Toxicology, 14(12), 1215–1229. doi: 10.1080/08958370290084872

27 Kulle, T.J., Sauder, L.R., Shanty, F., Kerr, H.D., Ferrell, B.P., Miller, W.R., & Milman, J.H. (1984). Sulfur Dioxide 

and Ammonium Sulfate Effects on Pulmonary Function and Bronchial Reactivity in Human Subjects. American 

Industrial Hygiene Association Journal, 45(3), 156–161. ISSN:1542-8125
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levels in the Valley. Pulmonary function tests were performed to assess the response 

of these exposures. No significant changes in pulmonary function or bronchial reactivity 

were observed immediately after the individual exposures or 24 hours after exposure. 

In an experimental study that also exposed rats to 500 μg/m

3

of sulfate for four to eight 

months, modest pulmonary impacts were noted.28 After four months, cellular 

immunologic responsiveness was not impaired, but physiologic changes were detected, 

including enlargement of bronchial epithelial (surface) cells and in alveolar size. 

For each of these studies, the modest health impacts observed at very high exposure 

levels are consistent with the low intrinsic toxicity of sulfate. This is consistent with 

results of a review of the epidemiological and toxicological research on sulfate.

29

Researchers found that PM sulfate was a weaker indicator of health risk than PM2.5 

mass. Because sulfate is correlated with PM2.5 mass, this result is inconsistent with 

sulfate having a strong health influence. The study concluded that the epidemiologic 

and toxicologic evidence provide little or no support for a causal association of sulfate 

and health risk at ambient concentrations.

Geological: Winter season and annual average PM2.5 found in the Valley contains a 

very small fraction of species that are termed crustal, i.e. having their origins in the 

earth’s crust. This coarse fraction—PM 2.5-10—contains a much higher fraction, as do 

particles beyond the PM10 size category. Suspended dust consists mainly of oxides of 

aluminum, silicon, calcium, titanium, iron, and other metal oxides. The precise 

combination of these components depends on the geology, industrial, and agricultural

processes of the area. Geological material typically consists of 5% to 15% PM 

particles.

Other researchers examined the respiratory inflammation potential of PM2.5 soil dust 

taken from nine different sites in the western U.S. taken from windblown dust and 

vehicle-generated particles from unpaved roads.30 None of the sites were located in the 

Valley. Cultured human epithelial cells were exposed and then were assessed for their 

release of cytokines known to be triggered by oxidative stress. PM2.5 from five of the 

sites was found to be benign, three of the sites demonstrated measurable cytokine 

response, and PM2.5 from one site was found to be highly reactive. Endotoxin, a 

potentially reactive bio-aerosol that is often found in PM, was not found to be a 

contributing factor to the variations in inflammatory potential. 

Although not technically a geologic species, respirable road dust (RRD) has been 

recognized and analyzed as a separate form of PM2.5 that has relevance to exposure 

 

28 Smith, L.G., Busch, R.H., Buschbom, R.L., Cannon, W.C., Loscutoff, S.M., & Morris, J.E. (1989). Effects of Sulfur 

Dioxide or Ammonium Sulfate Exposure, Alone or Combined, for 4 or 8 Months on Normal and Elastase-Impaired 

Rats. Environmental Research 49(1), 60-78. doi: 10.1016/S0013-9351(89)80022-2

29 Reiss, R., Anderson, E.L., Cross, C.E., Hidy, G., Hoel, D., McClellan, R., Moolgavkar, S. (2007). Evidence of 

Health Impacts of Sulfate-and Nitrate-Containing Particles in Ambient Air. Inhalation Toxicology, 19(5), 419-449.

doi:10.1080/08958370601174941

30 Veranth, J., Rielly, C.A., Veranth, M.M., Moss, T.A., Langelier, C.R., Lanza, D.L., & Yost, G.S. (2004). Inflammatory 

Cytokines and Cell Death in BEAS-2B Lung Cells Treated with Soil Dust, Lipopolysaccharide, and Surface-Modified 

Particles. Toxicological Science 82(1), 88–96. Retrieved from 

http://toxsci.oxfordjournals.org/content/82/1/88.full.pdf+html doi: 10.1093/toxsci/kfh24
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characterization of sources in this plan. In this context, RRD is defined as PM less than 

2.5 microns in diameter that is deposited along paved roadways as a result of roadway 

breakdown, tire wear, brake wear, deposition of exhaust-related particles, and other 

anthropogenic sources. Speciation analysis31 of RRD in southern California identified

over 100 organic compounds including n-alkanes, n-alkanoic acids, n-alkenoic acids, nalkanals, n-alkanols, benzoic acids, benzaldehydes, polyalkylene glycol ethers, PAH, 

oxy-PAH, steranes, hopanes, natural resins, and other compound classes. This 

relatively toxic mix of OC species is coincident with a range of metals associated with 

motor vehicle exhaust and component wear. RRD particles are re-suspended by 

passing traffic, leaf blowers, and other sources for possible inhalation by individuals in 

or near the roadway. 

To conclude, the geologic fraction of PM2.5 found in the Valley makes a relatively small 

contribution to overall PM2.5 mass and, by itself, has relatively low toxicity. RRD, while 

not of geologic origins, has been reviewed here because of its relevance to subsequent 

exposure characterization of sources in subsequent chapters.

2.4.3 Particle Size and Deposition

Particle size has a significant bearing on bodily deposition, net exposure, and 

corresponding health risk, even within the PM2.5 size fraction. Key metrics for 

deposition assessment include the percentage of inhaled particles that remain 

deposited and not exhaled (known as the deposition fraction) and the location where 

particles are deposited within the body).32 Within the PM2.5 size range, particles less 

than 0.1 microns (PM 0.1) and greater than 10 microns are least likely to be exhaled, 

and thus have higher deposition fractions.33 

The relationship between particle size, zone of deposition, and deposition fraction are 

depicted in Figure 2-2 and is summarized as follows:

A. Nasal, pharyngeal, laryngeal: As shown in Figure 2-2 at the upper right, the 

uppermost segment of the respiratory tract is the primary zone of deposition for 

the smallest and largest particles. Approximately 80% of extremely small 

particles of one nanometer (0.001 micron) diameter or less are retained here with 

a comparable deposition fraction in the 10 micron diameter.

B. Tracheobronchial: The deposition fraction in this zone peaks at nearly 40% 

for particles with diameters between 1 and 10 nanometers. Almost 100% of the 

particles above the PM 0.1 size cut are either deposited in the other two 

deposition zones or exhaled.

 

31 Rogge, W. F., Hildemann, L. M., Mazurek, M. A., Cass, G. R. and Simoneit, B. R. T. (1993). Sources of Fine 

Organic Aerosol—3. Road Dust, Tire Debris, and Organometallic Brake Lining Dust—Roads As Sources and Sinks. 

Environmental Science & Technology 27(9), 1892-1904.

32 International Commission on Radiological Protection [ICRP]. (1995). Human Respiratory Tract Model for 

Radiological Protection. ICRP Publication 66.. Annals of the ICRP 24, 1–3.

33 U.S. Environmental Protection Agency [EPA]. (2004, October). Air Quality Criteria for Particulate Matter: Final 

Report. Washington, D.C.: EPA 600/P-99/002aF-bF. Available at 

http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=87903
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C. Alveolar: Deposition in the gas exchange zone of the lungs peaks in the 10 

nanometer size with a gradual dissipation of deposition beyond the PM 0.1 size.

Figure 2-2 Relationships Between Particle Size Distribution and Respiratory 

 Deposition Zones

Deposition of very small particles in the alveolar region of the lungs results in the 

delivery of their chemicals into the bloodstream where they promote cardiovascular 

disruption and immune system sensitization.34 These chemicals can trigger heart 

attacks and premature death among individuals with pre-existing heart conditions.35 

Extremely small particles can also be absorbed into the brain via the nasal tract, 

 

34 Delfino, R.J., Sioutas, C., & Malik, S. (2005). Potential Role of Ultrafine Particles in Associations between Airborne 

Particle Mass and Cardiovascular Health. Environmental Health Perspectives 113(8), 934–946. Retrieved from 

http://ehp03.niehs.nih.gov/article/fetchArticle.action?articleURI=info%3Adoi%2F10.1289%2Fehp.7938

35 Nel A. (2005). Air Pollution-Related Illness: Effects of Particles. Science, 308(5723), 804–806. doi:

10.1126/science.1108752
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bypassing the protection provided by the blood-brain barrier.36 The effects of particles 

deposited primarily in the tracheobronchial region center on respiratory function.37

As depicted in Figure 2-3, particle deposition and associated health risk is magnified by 

exercise in several ways. First, the amount of inhaled air per minute rises substantially 

when breathing faster and more deeply. Second, breathing harder means that particles,

especially PM 0.1, are more likely to penetrate the alveolar region of the lungs where 

absorption into the bloodstream occurs. A 2003 study38 found that during moderate 

exercise 80% of inhaled PM 0.1 was deposited in the lungs, compared with 60% lung 

retention while at rest (see left panel in Figure 2-3). However, because the volume of 

air exchanged per minute increases substantially during exercise, overall PM 0.1 

deposition increased by 450% (right panel). Discussed further below, this phenomenon 

underscores the health risk posed to individuals who work or exercise in areas where 

sources of hydrocarbon combustion result in very high PM 0.1 particle concentrations. 

Figure 2-3 Particle Number Deposition Fraction (DF) and Total Particle 

Deposition of PM 0.1 at Rest and Exercise

 

36 Oberdorster, G., Sharp, Z., Atudorei, V., Elder, A., Gelein, R., Kreyling, W., & Cox, C. (2004). Translocation of 

Inhaled Ultrafine Particles to the Brain. Inhalation Toxicology, 16(6-7), 437–445.

37 U.S. Environmental Protection Agency [EPA]. (2009). Integrated Science Assessment for Particulate Matter: Final 

Report. Washington, D.C.: EPA/600/R-08/139F. Available at 

http://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=216546

38 Daigle, C., Chalupa, D.C., Gibb, F.R., Morrow, P.E., Oberdörster, G., Utell, M.J., & Frampton, M.W. (2003).

Ultrafine Particle Deposition in Humans during Rest and Exercise. Inhalation Toxicology, 15(6), 539–552. doi:

10.1080/08958370304468
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2.4.4 Exposure to Ultrafine Particles (PM 0.1) 

Elevated exposure to freshly emitted PM 0.1 is a critical health risk factor that often 

does not correspond to ambient PM2.5 concentrations at local monitors. PM 0.1 are 

formed through nucleation and gas-to-particle reactions and grow (or shrink) through a 

number of mechanisms including condensation, coagulation, and volatilization.39 High 

concentrations of primary (directly emitted) PM 0.1 are typically found near fresh 

sources of hydrocarbon combustion, including coal plants, charbroiled meat, diesel and 

gasoline vehicles, wood combustion, and lawn care equipment. These combustion

particles start out very small, grow larger over time and space, and evolve chemically at 

the same time. Secondary PM 0.1 typically is formed via particle nucleation from gas or 

liquids and are characterized by larger geographic scales and more uniform population 

exposure. 

Despite being extremely small, PM 0.1 has an extremely high surface area, as seen in 

Figure 2-4. Compared to an equal mass of particles of two microns (PM 2.0) in 

diameter, ultrafine particles that are 1,000 times smaller (20 nanometers or PM 0.02) 

nonetheless have 125 times the surface area.40 In addition, PM 0.1 produced by 

hydrocarbon combustion typically contain a rich mixture of chemicals with potential 

health effects, including nickel, iron, vanadium, PAH, and others.41 Chemical potency, 

very high surface area, and alveolar deposition are signal characteristics of PM 0.1 from 

hydrocarbon combustion that result in significant health risks from chronic exposure. 

Figure 2-4 Electron Micrograph of an Ultrafine Particle42 

 

39 Solomon, P. (2012). An Overview of Ultrafine Particles in Ambient Air. EM: Journal of the Air & Waste Management 

Association, May, 18–26.

40 Donaldson, K., Stone, V., Clouter, A., Renwick, L., & MacNee W. (2001). Ultrafine Particles. Occupational 

Environmental Medicine 58, 211–216.Retrieved from http://oem.bmj.com/content/58/3/211.short doi:

10.1136/oem.58.3.21

41 Morawska, L., Ristovski, Z., & Jayaratne, E.R. (2008). Ambient Nano and Ultrafine Particles from Motor Vehicle 

Emissions: Characteristics, Ambient Processing and Implications on Human Exposure. Atmospheric Environment,

42(35), 8113–8138. doi: 10.1016/j.atmosenv.2008.07.050

42 Nel A. (2005). Air Pollution-Related Illness: Effects of Particles. Science, 308(5723), 804–806. doi:

10.1126/science.1108752
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Sub-populations who live or work near sources of primary PM 0.1 from hydrocarbon 

combustion are particularly at risk. Health scientists have generated an overwhelming 

body of epidemiological (statistical) evidence that individuals near freeways (less than 

300 meters) are being harmed via chronic inhalation of PM 0.1 from vehicles.43 

Similarly, a recent study of residential wood burning in Cambria, California found very

high neighborhood concentrations of PM 0.1 from wood smoke even though 

concentrations of PM2.5 at the nearby ambient monitor met the federal health 

standard.44 The health risk from fresh sources of PM 0.1 has important environmental 

justice implications to the extent that elevated exposure to near-source PM 0.1 is 

concentrated in communities that already face sources of risk related to race or 

socioeconomic status.45 Chronic exposure to near-source PM 0.1 commonly occurs in 

locations where local monitors are in attainment for PM2.5 standards and during 

seasons when ambient PM2.5 concentrations are below the annual daily standard of 15 

μm/m3.

2.4.5 Population Proximity and Intake Fraction 

Estimating total exposure and net health risk from a given source of PM2.5 requires that 

population proximity and population density be considered in addition to the source’s 

contribution to the regional PM2.5 emissions inventory and its toxicity. In addition to 

factors governing net deposition of inhaled particles reviewed above, net population 

exposure from the source in question is also shaped by the number of exposed 

individuals who inhale the emissions and the duration of exposure in conjunction with 

aerosol concentration levels (see Figure 2-5). Known as the intake fraction, this 

measure of population exposure is defined empirically as the pollutant mass inhaled 

divided by the mass emitted.46 Intake fraction is useful in connecting emissions to 

health risk because the mass inhaled is a better indicator of health risk than the mass 

emitted or airborne concentration. Two different pollutant sources with very comparable 

emission rates of the same pollutant can nonetheless have significantly different intake 

fractions depending on the surrounding population density. For example, sources of 

PM2.5 located in rural areas may have an intake fraction that is 10 to 100 times smaller 

than a comparable source located within a densely populated city. 

 

43 Gauderman, W., Vora, H., McConnell, R., Berhane, K., Gilliland, F., Thomas, ... Peters, J. (2007). Effect of 

Exposure to Traffic on Lung Development from 10 to 18 Years of Age: A Cohort Study. The Lancet 369(9561), 571–

577. Retrieved from http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(07)60037-3/fulltext#article_upsell

44 Thatcher, T. & Kirchstetter, T. (2011). Assessing Near-Field Exposures from Distributed Residential Wood Smoke 

Combustion Sources. Report prepared for the California Air Resources Board. Retrieved from 

http://www.arb.ca.gov/research/rsc/10-28-11/item2dfr07-308.pdf

45 London, J., Huang, G., & Zagofsky, T. (2011). Land of Risk, Land of Opportunity: Cumulative Environmental 

Vulnerabilities in California’s San Joaquin Valley. Davis, CA: University of California, Davis, Center for Regional 

Change. Retrieved from 

http://regionalchange.ucdavis.edu/publications/Report_Land_of_Risk_Land_of_Opportunity.pdf

46 Marshall, J.D., & Nazaroff, W.W. (2004, October). Using Intake Fraction to Guide ARB Policy Choices: The Case of 

Particulate Matter. Unpublished California Air Resources Board Report.
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Figure 2-5 Simplified Intake Fraction Model

The relevance of the intake fraction concept can be seen in a recent study of 

neighborhood variability in wood smoke concentrations in Cambria, California.47 As 

described above, the winter study found very high concentrations of PM 0.1 on a 

neighborhood scale that were often not reflected in PM2.5 concentrations measured by 

local air quality monitors. In effect, a single wood-burning household had the effect of 

enveloping the adjacent and downwind homes with a PM 0.1 plume. Furthermore, the 

study also found that wood smoke PM 0.1 was infiltrating adjacent homes that were not 

burning, with an average indoor concentration found to be 74% as high as immediately 

outside the homes. Taking into consideration the length of PM 0.1 inhalation during 

sleeping hours, the relatively high concentration of PM 0.1 found in the plume, and the 

number affected of individuals in an urban neighborhood, the intake fraction resulting 

from the source of the wood smoke would be very high. Assuming that this nightly 

exposure occurred over the course of a season, the cumulative health risk to the 

neighborhood would be considerable and would almost certainly exceed the risk 

indicated by daily concentrations of PM2.5 measured by ambient monitors.

 

47 Thatcher, T. & Kirchstetter, T. (2011). Assessing Near-Field Exposures from Distributed Residential Wood Smoke 

Combustion Sources. Report prepared for the California Air Resources Board. Retrieved from 

http://www.arb.ca.gov/research/rsc/10-28-11/item2dfr07-308.pdf
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2.5 HEALTH BENEFITS ACHIEVED THROUGH 2012 PM2.5 PLAN

Understanding the results of any strategy is critical to assessing the overall value and 

success of that strategy. As part of integrating the Risk-Based Strategy into this plan, 

the District has estimated the fundamental metric associated with implementation of the 

2012 PM2.5 Plan – the health benefits resulting from implementation of this strategy. 

As presented below and described in more detail in Appendix E, an EPA-developed 

model called BenMAP has been employed in order to estimate the annual reductions in 

morbidity (disease) and mortality (premature death) attributable to improved air quality 

due to the 2012 PM2.5 Plan in the attainment year of 2019.

BenMAP is a sophisticated computer software model developed by the U.S. EPA that is 

well-suited for estimating the health benefits from the 2012 PM2.5 Plan. Over the 

course of the past decade, ongoing progress in the fields of epidemiology and 

geographic information systems (GIS) have resulted in the development of computer 

models that are capable of estimating the health benefits of improved air quality with 

reasonable accuracy when properly applied. These models estimate the number of 

avoided cases of certain diseases and other health impairment categories, known as 

health endpoints, which result from a specified reduction in exposure to criteria air 

pollutants, in this case, reduced exposure to PM2.5 concentrations. 

Through implementation of the comprehensive control strategy included in this plan and 

the resulting reductions in PM2.5 concentrations throughout the Valley, the District 

estimates the following health benefits using this model:

Table 2-1: Health Benefits Achieved Through Implementation of the Plan

Health Impact Health Benefit 

(reduction in health impact) 

Premature Death 671

Acute Myocardial Infarction, Hospital Admissions 93

Asthma Age 0-19, Hospital Admissions 131

Cardiovascular, Hospital Admissions 175

Asthma Age 20-99, Hospital Admissions 246

Asthma Age 20-99, Emergency Room Visits 407

Asthma Age 0-19, Emergency Room Visits 699

Acute Bronchitis 1,498

Upper Respiratory Symptoms 15,523

Lower Respiratory Symptoms 19,011

Asthma Exacerbation 114,376

Work Loss Days 125,138

In addition to quantifying reductions in disease and death based on improvements in 

county-level PM2.5 concentrations, BenMAP can also be used as a tool to quantify the 

economic benefits associated with quantified health benefits. While assigning economic 
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values to health impacts is difficult given the tremendous social values associated with 

these impacts, BenMAP attempts to assign values using an existing body of literature 

that connects impacts to hard costs such as lost wages, or, in the case of premature 

death, a social value of $7.99 million per incidence. Using this model, the District 

estimates that implementation of the plan will achieve an annual Valley-wide savings of 

$102 million in health costs in 2019 , as outlined in the following table. Additionally, and 

more significantly, a social benefit of $5.36 billion is estimated for the 671 avoided 

premature deaths. 

Table 2-2: Economic Costs Associated with Quantified Health Benefits

Health Impact Health Benefit 

(reduction in health impact) 

Hospital Admissions, Respiratory $386,955

Asthma, Emergency Room Visits $429,496

Acute Bronchitis $717,759

Acute Myocardial Infarction $3,081,686

Upper Respiratory Symptoms $3,677,083

Lower Respiratory Symptoms $4,502,994

Asthma, Hospital Admissions $6,279,033

Cardiovascular, Hospital Admissions $6,767,955

Asthma Exacerbation $10,660,442

Work Loss Days $19,539,004

Acute Respiratory Symptoms $46,109,557

Total $102,151,964
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