Chapter 3

Health	Impacts	and	the	Health	Risk	Reduction	

Strategy	

2015 Plan for the 1997 PM2.5 Standard

SJVUAPCD	

 

 
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Chapter 3: Health Impacts and the Health Risk Reduction Strategy 

2015 Plan for the 1997 PM2.5 Standard

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3-1 Chapter 3: Health Impacts and the Health Risk Reduction Strategy 

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Chapter 3: Health Impacts and the Health Risk Reduction Strategy 

Particulate matter (PM) is a mixture of solid particles and liquid droplets in the air. PM 

can be emitted directly into the atmosphere (primary PM), or can form as secondary 

particulates in the atmosphere through the photochemical reactions of precursors (when 

precursors are energized by sunlight). Thus, PM is made up of a number of 

components, including acids (such as nitrates and sulfates), organic chemicals, metals, 

and soil or dust particles. PM10 is particulate matter that is 10 microns or less in 

diameter, and the PM2.5 subset includes smaller particles that are 2.5 microns or less 

in diameter (Figure 3-1). 

Figure 3-1 Visual Comparison of PM10, PM2.5, Human Hair, and Fine Beach Sand 

3.1 PM2.5 AND ASSOCIATED HEALTH IMPACTS 

Any particles 10 microns or less are considered respirable, meaning they can be 

inhaled into the body through the mouth or nose. PM10 can generally pass through the 

nose and throat and enter the lungs. PM2.5 can be inhaled more deeply into the gas 

exchange tissues of the lungs, where it can be absorbed into the bloodstream and 

carried to other parts of the body. 

The potential health impacts of particle pollution are linked to the size of the particles, 

with the smaller particles having larger impacts. Numerous studies link PM2.5 to a 

variety of health problems, including aggravated asthma, increased respiratory 

symptoms (irritation of the airways, coughing, difficulty breathing), decreased lung 

function in children, development of chronic bronchitis, irregular heartbeat, non-fatal 

heart attacks, increased respiratory and cardiovascular hospitalizations, lung cancer, 

and premature death. Children, older adults, and individuals with heart or lung diseases 

are the most likely to be affected by PM2.5. Many studies have quantified and 
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3-2 Chapter 3: Health Impacts and the Health Risk Reduction Strategy 

2015 Plan for the 1997 PM2.5 Standard

documented the health benefits of attaining the U.S. Environmental Protection Agency 

(EPA) air quality standards for PM. For example, one 2008 study used the Regional 

Human Exposure Model (REHEX) to evaluate potential San Joaquin Valley (Valley) 

health benefits.1

 

In addition to particle size, the chemical composition of PM2.5 is a primary factor in the 

type and severity of health impacts. There are several PM2.5 species or chemical 

compounds, as summarized in the following table. 

Table 3-1 Summary of PM2.5 Species 

PM2.5 Species Description 

Organic carbon 

Directly emitted, primarily from combustion sources (e.g. residential 

wood combustion). Also, smaller amounts attached to geologic material 

and road dusts. May also be emitted directly by natural/biogenic 

sources. 

Elemental carbon Also called soot or black carbon; formed during incomplete combustion 

of fuels (e.g. diesel engines). 

Geologic material Road dust and soil dust that are entrained in the air from activity, such 

as soil disturbance or airflow from traffic. 

Trace metals 

Identified as components from soil emissions or found in other 

particulates having been emitted in connection with combustion from 

engine wear, brake wear, and similar processes. Can also be emitted 

from fireworks. 

Sea salt Sodium chloride in sea spray where sea air is transported into the 

Valley. 

Secondary organic 

aerosol 

Secondary particulates formed from photochemical reactions of organic 

carbon. 

Ammonium nitrate 

Reaction of ammonia and nitric acid, where the nitric acid is formed from 

nitrogen oxide emissions, creating nitric acid in photochemical

processes or nighttime reactions with ozone. 

Ammonium sulfate 

Reaction of ammonia and sulfuric acid, where the sulfuric acid is formed 

primarily from sulfur oxide emissions in photochemical processes, with 

smaller amounts forming from direct emissions of sulfur. 

Combined water A water molecule attached to one of the above molecules. 

Understanding various PM2.5 species, including how each species is formed, how 

much each contributes to the Valley’s total PM2.5 concentrations, and how each is 

linked to different public health impacts, is of the utmost importance for the development 

of an effective, health-protecting control strategy. For example, ammonium nitrate is 

estimated to comprise about 40% of the Valley’s annual average PM2.5 concentrations, 

but it is generally regarded as having relatively low toxicity as compared to other types 

of PM2.5 species. In contrast, metals have greater health impacts, but are found in 

relatively low concentrations in the Valley. Bioaerosols, such as mold spores, bacteria, 

pollen, and endotoxins, carry significant health risks for sensitive individuals. Ultrafine 

 

1

 Hall, J.V., Brajer, V., Lurmann, F.W. (November 2008). The Benefits of Meeting Federal Clean Air Act Standards in 

the South Coast and San Joaquin Valley Air Basins. Institute for Economic and Environmental Studies, California 

State University, Fullerton. Retrieved from 

http://business.fullerton.edu/centers/iees/reports/Benefits_of_Meeting_Clean_Air_Standards_11-13-08.pdf
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3-3 Chapter 3: Health Impacts and the Health Risk Reduction Strategy 

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particles, or those particles 0.1 microns or less in diameter (PM0.1), are small enough to 

effectively deliver harmful chemicals into the lungs, bloodstream, and the brain, but 

typically comprise a very small portion of the Valley’s total airborne PM mass. 

In addition to affecting human health, air pollution also affects the health of the natural 

environment. PM2.5 can be transported from sources hundreds of miles away to 

contribute to visibility problems at remote locations, such as the Sierra Nevada 

mountain range and associated national parks. As PM settles out of the air, it can make 

lakes and streams acidic, change an ecosystem’s nutrient balance, and affect 

ecosystem diversity. PM can affect vegetation by damaging foliage, disrupting the 

chemical processes within plants, reducing light adsorption, and disrupting 

photosynthesis. This can impact green spaces as well as crops. PM can also stain and 

damage stone and other materials. As the Valley progresses toward attainment of 

EPA’s human-health-based PM2.5 standards, there will also be less harmful impacts to 

the surrounding natural environment. 

3.2 WHAT IS THE HEALTH RISK REDUCTION STRATEGY? 

The 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. 

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 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.2

 

 

2

 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
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EPA policy directly acknowledges the importance of a health risk reduction-based 

strategy to maximize public health benefits within a region’s efforts to attain the 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...”

3

 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 pollutants, such as 

SO2 and NOx,4 and providing methods to maximize health benefits and minimize risk 

inequality.5 

The San Joaquin Valley Air Pollution Control District (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 was to minimize cumulative population exposure to air 

pollution and corresponding health risks in the region. In May 2013, the District 

Governing Board rebranded this strategy as the Health Risk Reduction Strategy 

(HRRS) in response to criticisms and skepticism by a number of air quality advocates, 

even though the air quality advocates did not put forward any scientific or policyrelevant evidence to refute the RBS, and the fact that the RBS had been steadily 

gaining support from both the EPA and the scientific community. Even industry 

representatives largely embraced the RBS, even though it targets certain sources for 

new air pollution control strategies. This is largely due to the fact that the RBS provides 

an assurance of effective controls that produce real air quality benefits. The District has 

integrated the HRRS into the development of air quality attainment plans. 

3.3 BACKGROUND FOR THE HEALTH RISK REDUCTION 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. 

 

3

 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

4

 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 

5

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

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

harmful and have pinpointed their sources.6 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 HRRS. Rather than ignore 

this growing body of scientific knowledge, the District’s HRRS 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 of federal standards. The outcome is stronger, more health-protective plans 

that reflect the current trajectory of scientific knowledge toward a more complete 

understanding of population risk from PM2.5 particles. 

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

scenario. The HRRS 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. 

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

and goals of the HRRS 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 

 

6

 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.7 

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. 

Similarly, the District’s 2012 PM2.5 Plan committed to amend the District Rule 

4901 in 2016 with compliance beginning the winter season of 2016-2017 with an 

estimated 1.5 tons per day (tpd) of PM2.5 emission reductions. When the District 

Governing Board adopted the 2012 PM2.5 Plan, guided by the HRRS, they 

directed the District to amend Rule 4901 in 2014. As a result, the District’s 

residential wood burning program was amended in September 2014 with 

implementation in the winter season of 2014-2015, two years ahead of the SIP 

commitment. The rule was further strengthened and the curtailment threshold 

lowered to 20 μg/m3

. The combination of the lowered curtailment threshold, 

tiered curtailments, increased public outreach and education, and increased 

incentive amounts and allocations result in a much greater estimated reduction of 

directly emitted PM2.5 emissions during the winter season than the previously 

estimated amount of 1.5 tpd. 

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 HRRS. 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. 

 

7

 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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 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 close to 4,000 high-polluting gas-powered lawn mowers with clean 

electric mowers, and through the Burn Cleaner Incentive Program, the District 

has replaced over 6,000 high-polluting wood burning devices with cleaner 

alternatives. These grant programs result in a decrease in urban, localized 

health risks associated with the use of gas-powered equipment and wood 

burning devices. 

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

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 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. As part of the District’s 

HRRS, the District is playing an active role in funding leading edge health 

research focusing on the Valley population. In 2010–2011, the District 

sponsored the first major epidemiological investigation of health effects of air 

pollution in the Valley, focusing on the populations of Modesto, Fresno, and 

Bakersfield.8

 The study found that daily exposure to high PM2.5 concentrations 

was significantly correlated with increased daily hospital and emergency room 

admission rates for asthma and other respiratory and cardiovascular diseases. 

In 2012, the District sponsored a follow-up epidemiological study to examine 

which of the chemical species found in Valley PM2.5 are most highly correlated 

with elevated ER and hospital admission rates. Results are expected to be 

published in the near future. In 2010, the District sponsored a pilot study of PM 

0.1 aka ultrafine particles in Fresno. UCSF-Fresno investigated the quantity and 

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

wood burning, and restaurants. Currently the District is funding a UC Davis 

research project to develop a model of PM0.1 population exposure in the Valley 

based on previous Valley observational research. PM0.1 exposure will be 

correlated with short- and long-term health effects by making use of the large 

body of Valley epidemiological data that has been generated by the previous 

studies described above. The District will continue to seek out and fund research 

opportunities that further the understanding of PM-related impacts on public 

health. 

 

8

 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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3.4 FIVE-FACTOR EXPOSURE ASSESSMENT METHODOLOGY 

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

HRRS is implemented in air quality attainment plans employing a scientifically based 

exposure characterization methodology that draws on the latest scientific understanding 

about health risk from PM2.5 exposure. 

The District uses a five-factor exposure assessment methodology under the HRRS: 

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 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 

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. 

3.4.1 Relevance to Attainment 

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

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

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

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. 

3.4.2 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 
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despite comparable regional PM2.5 mass exposure.9 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.10 

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, 

ammonium sulfate, and geological. PM2.5 is regularly speciated at several Valley 

monitoring sites. 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.11 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.12 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.13 Low molecular weight PAH is found in other 

 

9

 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 10 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

11 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 12 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 13 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 
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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.14 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 

correlated with sustained (multi-day) high ambient concentrations of PM2.5 and was 

accompanied by decreased lung function.15 

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.16 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.17 A recent study in Mexico City found an 

association between exposure levels of EC and lung function decrements among 

asthmatic and non-asthmatic children.18 

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 

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

doi:10.1016/J.tox.2006.12.009

14 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 15 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). 16 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. 17 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 18 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. 
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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.19 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. 

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.20 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.21 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.22 

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.23

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 during multiday stagnation 

events. As seen in the following figure, nitrate is significant because it can contribute up 

to almost 40% of PM2.5 mass on an annual average day basis. 

 

19 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 20 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 21 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/ 22 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 23 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
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Figure 3-2 Annual Average PM2.5 Chemical Composition 

 

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. 

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.24 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. 

 

24 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 
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One experimental study was found that explicitly looked for toxic mechanisms driven by 

ammonium nitrate.25 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. Mass concentrations of sulfate are significantly lower than for 

nitrate in the Valley, averaging from 10% to 11% of PM2.5 mass on an annual average 

basis. 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 study26 examined the response of 20 

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

μg/m3 of sulfate aerosol, a concentration over two orders of magnitude above ambient 

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/m3 of sulfate for four to eight 

months, modest pulmonary impacts were noted.27 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.28 

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 

 

25 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 26 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 27 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 28 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 
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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 

from windblown dust and vehicle-generated particles from unpaved roads, taken from 

nine different sites in the western U.S.29 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 

characterization. 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 analysis30 of RRD in southern California identified over 100 organic 

compounds including n-alkanes, n-alkanoic acids, n-alkenoic acids, n-alkanals, nalkanols, 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. 

 

29 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 30 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. 
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3.4.3 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).31 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.32 

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

depicted in the following figure and is summarized as follows: 

 Nasal, pharyngeal, laryngeal: 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. 

 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. 

 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. 

 

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

Radiological Protection. ICRP Publication 66.. Annals of the ICRP 24, 1–3. 32 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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Figure 3-3 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.33 These chemicals can trigger heart 

attacks and premature death among individuals with pre-existing heart conditions.34 

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

bypassing the protection provided by the blood-brain barrier.35 The effects of particles 

deposited primarily in the tracheobronchial region center on respiratory function.36

 

33 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 34 Nel A. (2005). Air Pollution-Related Illness: Effects of Particles. Science, 308(5723), 804–806. doi: 

10.1126/science.1108752 

35 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. 36 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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As depicted in Figure 3-4, 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 study37 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 3-4). However, because the volume of 

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

deposition increased by 450% (right panel). 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 3-4 Particle Number Deposition Fraction (DF) and Total Particle 

Deposition of PM0.1 at Rest and Exercise 

3.4.4 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.38 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 

 

37 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 

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

Association, May, 18–26. 
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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 is 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 3-5. 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.39 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.40 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 3-5 Electron Micrograph of an Ultrafine Particle41

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.42 

Similarly, a 2011 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 

 

39 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 

40 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 41 Nel A. (2005). Air Pollution-Related Illness: Effects of Particles. Science, 308(5723), 804–806. doi: 

10.1126/science.1108752 

42 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
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standard.43 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.44 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. 

3.4.5 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 3-6). Known as the intake fraction, this 

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

divided by the mass emitted.45 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. 

Figure 3-6 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.46 The 

 

43 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 44 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 45 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. 46 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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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. 

3.5 HEALTH BENEFITS ACHIEVED BY REDUCING PM2.5 EMISSIONS 

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

and success of that strategy. 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. 

EPA developed a sophisticated computer software model called BenMAP that is wellsuited for estimating health benefits and that can therefore be employed in order to 

estimate the annual reductions in morbidity (disease) and mortality (premature death) 

attributable to improved air quality due. As the District continues to develop air quality 

attainment plans in future years to address the increasingly stringent NAAQS, the 

District will evaluate health benefits for Valley residents resulting from adopted air 

quality attainment plans.