# Chapter 3

Health	Impacts	and	the	Health	Risk	Reduction Strategy

2015 Plan for the 1997 PM2.5 Standard SJVUAPCDSan Joaquin Valley Unified Air Polluti on Control District April 16, 2015

Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard This page intentionally blank.

.San Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-1 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard 

### Chapter 3: Health Impacts and th e Health Risk Reduction Strateg y

Particulate matter (PM) is a mixt ure of solid particles and liq uid droplets in the air. PM can be emitted directly into t he atmosphere (primary PM), or ca n form as secondary particulates in the atmosphere through the photochemical reacti ons of precursors (when precursors are energized by sunli ght). Thus, PM i s made up of a number of components, including acids (such as nitrates and sulfates), or ganic chemicals, metals, and soil or dust particles. PM10 is particulate matter that is 10 microns or less in diameter, and the PM2.5 subset i ncludes 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 F ine Beach Sand

3.1 PM2.5 AND ASSOCIATED HEALTH IMPACTS

Any particles 10 microns or less are considered respirable, mea ning they can be inhaled into the body through the mouth or nose. PM10 can gene rally pass through the
nose and throat and enter the l ungs. PM2.5 can be inhaled more deeply into the gas exchange tissues of the lungs, whe re it can be absorbed into th e bloodstream and
carried to other parts of the body.

The potential health impacts of p article pollution are linked t o the size of the particles, with the smaller particles havi ng larger impacts. Numerous stu dies link PM2.5 to a variety of health problems, inc luding aggravated asthma, increa sed respiratory symptoms (irritation of the airw ays, coughing, difficulty breat hing), decreased lung function in children, developmen t of chronic bronchitis, irregu lar heartbeat, non-fatal heart attacks, increased respirat ory and cardiovascular hospita lizations, lung cancer, and premature death. Children, o lder adults, and individuals w ith heart or lung diseases are the most likely to be affect ed by PM2.5. Many studies have quantified andSan Joaquin Valley Unified Air Polluti on Control District April 16, 2015

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 a ttaining the U.S. Environmen tal Protection Agency (EPA) air quality standards for PM. For example, one 2008 stud y used the Regional Human Exposure Model (REHEX) to e valuate 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. resid ential wood combustion). Also, smaller amounts attached to geologic m aterial and road dusts. May also be emitted directly by natural/biogen ic

sources.

Elemental carbon Also called soot or black carbon; formed during incomplete comb ustion of fuels (e.g. diesel engines).

Geologic material Road dust and soil dust that are entrained in the air from acti vity, such
as soil disturbance or airflow from traffic.

Trace metals Identified as components from soil emissions or found in other particulates having been emitt ed in connection with combustion from engine wear, brake wear, and similar processes. Can also be em itted
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 o rganic
carbon.

Ammonium nitrate Reaction of ammonia and nitric acid, where the nitric acid is f ormed 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 emi ssions in photochemical processe s, with smaller amounts forming from direct emissions of sulfur.
Combined water A water molecule attached to one of the above mo lecules.

Understanding various PM2.5 species, inclu ding how each species is formed, how
much each contributes to the Vall ey’s total PM2.5 concentration s, and how each is linked to different public health impacts, is of the utmost imp ortance for the development of an effective, health-protect ing control strategy. For examp le, 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, me tals have greater health impa cts, but are found in relatively low concentrations in the Valley. Bioaerosols, such as mold spores, bacteria, pollen, and endotoxins, carry si gnificant health risks for sens itive individuals. Ultrafine

1 Hall, J.V., Brajer, V., Lurm ann, 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 Envi ronmental Studies, California State University, Fullerton. Retrieved from http://business.fullerton.edu/cent ers/iees/reports/Benefits_of_ Meeting_Clean_Air_Standards_11-13-08.pdfSan Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-3 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard particles, or those particles 0.1 microns or less in diameter ( PM0.1), are small enough to effectively deliver harmful chem icals into the lungs, bloodstre am, and the brain, but typically comprise a very small portion of the Valley’s total a irborne PM mass.

In addition to affecting human heal th, air pollution also affec ts the health of the natural
environment. PM2.5 can be trans ported from sources hundreds of miles away to contribute to visibility problem s at remote locations, such as the Sierra Nevada mountain range and asso ciated national parks. As PM settles ou t of the air, it can make lakes and streams acidic, change an ecosystem’s nutrient balanc e, and affect ecosystem diversity. PM can af fect vegetation by damaging foli age, disrupting the chemical processes within plant s, reducing light adsorption, an d disrupting photosynthesis. This can impact g reen spaces as well as crops. PM can also stain and damage stone and other mat erials. As the Valley progresses tow ard attainment of
EPA’s human-health-bas ed PM2.5 standards, t here will also be le ss harmful impacts to the surrounding natural environment.

3.2 WHAT IS THE HEALTH R ISK REDUCTION STRATEGY?

The EPA National Ambient Air Qua lity Standards (NAAQS) are the primary driving force
for new emissions controls that r esult in air quality improveme nts and health benefits to Valley residents. In the convent ional planning process for att aining these standards, success in protecting public heal th is defined by whether the s tandards are met at all air monitors. In effect, the reducti on in PM2.5 mass, which shows progress toward attainment of the standard, ser ves as the surrogate for populat ion exposure and risk.

Attaining these standards will re sult 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 d istribution, chemical species composition, surface a rea, and other factors of health risk. There is inherent complexity in documenting the health risks associated with expo sure to particles (which have a wide range of char acteristics) as com pared to pollutants like ozone (which has more consistency between molecules).

In contrast, recent health-scienc e research has substantially d eepened our knowledge of air pollutant health risk bey ond the current Clean Air Act ( CAA) framework and EPA standards. There is a growing re cognition within the scientifi c community that the NAAQS alone can be incomplete m easures of public exposure to ai r pollution. Thus, while the CAA NAAQS and state implementati on plan (SIP) process is motivated by public health, the process alone does not fully address public health impacts of ambient air pollution. To fully addre ss potential publi c health benefi ts, an attainment strategy can use a more comprehensive, mul tidimensional population expos ure assessment approach that goes beyond am bient mass measurements. 2

2 Lippman, M. (2012, April 16). Presentation: Results from Natio nal Particle Component Toxicity (NPACT) Program and NYU: Toxicology Findings, Int egration, and implications. Pr esented at the Annual Meeti ng of the Health Effects Institute (HEI) in Chicago, IL, A pril 15–17, 2012 . Presentation retrieved from http://www.healtheffects.org/Slides/AnnConf2012/Lippmann-MonPM. pdfSan Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-4 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard EPA policy directly acknowledges t he importance of a health ris k reduction-based strategy to maximize public hea lth benefits within a region’s e fforts to attain the NAAQS.
EPA’s March 2012 PM2.5 implementation guidance memo states, “...i t is likely that
SIPs for the 2006 24-hour PM2.5 N AAQS may need to include great er emphasis on reducing emissions from local sources

... ” 3 EPA’s memo further encourages that states consider evidence from published literature indicating that red uctions 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 maxim ize health benefits and minimize risk inequality. 5

The San Joaquin Valley Air Pollu tion Control District (District ) Governing Board adopted
a research-driven Risk-based Stra tegy (RBS) designed to maximiz e public health improvements resulting from the District’s attainment strategie s and related initiatives. The overall goal of the RBS was to minimize cumulative populati on exposure to air pollution and corresponding health risks in the region. In May 2013, the District Governing Board rebranded this str ategy as the Health Risk Redu ction Strategy (HRRS) in response to criticism s and skepticism by a number of air quality advocates, even though the air quality advocat es did not put forward any s cientific 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 embrac ed the RBS, even though it target s certain sources for new air pollution control stra tegies. This is largely due to t he fact that the RBS provides
an assurance of effective contro ls that produce real air qualit y benefits. The District has integrated the HRRS into the dev elopment of air quality attainm ent plans

.

3.3 BACKGROUND FOR THE HEALTH RISK REDUCTION STRATEGY

As a response to mounting epidemio logical evidence that PM2.5 w as more harmful than PM10, EPA established a PM2.5 NAAQS in 1997 to accompany the pr eviously established PM10 NAAQS. PM10 o ccurs at larger mass concentrati ons than PM2.5, so
the shift to PM2.5 somewhat conf licted with the time-tested tox icological precept of “the dose (mass) makes the poison.” P articulate inhalation studies found that the smaller PM2.5 particles penetrate more deeply into the lungs, where par ticles more effectively avoid immune system defenses. To xicological analyses of PM2.5 identified chemical species that acted differentially to promote respiratory and ca rdiovascular inflammation.
While it was unclear at that time which PM2.5 chemicals were th e most harmful, the
scientific consensus was that the health risks stemmed from the chemicals rather than the particles themselves.

3 U.S. Environmental Protection A gency (2012, March 2). Memorand um from the Office of Air Quality Pl anning and Standards: Implementation Guidance for the 2006 24- Hour Fine Pa rticle (PM2.5) Nationa l Ambient Air Quality Standards (NAAQS). Retrieved from http://www.epa.gov/ttn/naaqs/pm/pd fs/20120302_impl ement_guidanc e_24- hr_pm2.5_naaqs.pdf

4 Fann, N., Fulcher, C.M., & Hubbe ll, B.J. (2009). The Influence of Location, Source, and Em ission Type in Estimates
of the Human Health Benefits o f 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 I nequality: Incor porating Local- Scale Data in the Design a nd Evaluation of Air Quality
Policies. Risk Analysis, 31(6) , 908–922. doi: 10.1111/j.1 539-6924.2011.01629.xSan Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-5 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard In the years since the first PM2 .5 NAAQS was est ablished, scien tists have conducted
numerous studies that have identif ied which chemical species of PM2.5 are most harmful and have pinpointed their sources. 6 Health researchers have also documented the negative cardiovascular and i mmune system effects of ultraf ine particles, or particles that are 0.1 microns o r smaller (PM 0.1), based on th ese particles’ ability to penetrate the alveolar region o f the lungs and deliver chemical s into the bloodstream. This smaller-is-more-dangerous p henomenon parallels the previou s discovery regarding the higher toxicity of PM2.5 par ticles compared to larger and h eavier PM10 particles. In each case, the dose-makes-the-poi son assumption governing the N AAQS for carbon monoxide, lead, ozone, and the ot her criteria pollutants does n ot apply to particulates.

Addressing the complexity of heal th risks posed by particulate pollution has been a motivating factor in the devel opment and application of the HRR S. Rather than ignore this growing body of scientific knowledge, the District’s HRRS seeks to embrace it to the extent possible within the curr ent CAA to maximize public healt h benefits. In practice, this knowledge provides the Distr ict with the necessary scienti fic foundation for justifying and prioritizing the pollution cont rol measures that are necess ary for demonstrating
attainment of federal standards. The outcome is stronger, more health-protective plans that reflect the current traject ory of scientific knowledge tow ard a more complete understanding of population risk from PM2.5 particles.

The NAAQS-SIP proce ss and the HRRS are complimentary strategies , not an either-or
scenario. The HRRS should not be in terpreted as a zero-sum tra deoff that emphasizes
controls on certain forms and s ources of high-risk PM2.5 while ignoring others. The current mass-based indicator (micr ograms 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 program s have been influenced by the u nderlying principles and goals of the HRRS and provide a model of the success and ad ded potential benefits possible unde r this strategy.

 District Rule 4901 (W ood Burning Fireplaces and Wood Burning He aters) and the District’s corresponding Check-Before-You-Burn program have both been reducing harmf ul species of PM2.5 where and when thos e reductions are most needed—in impacted urbani zed areas when the local weat her is forecast to hamper PM dispersi on. By decreasing emissions from residential wood burning, Rule 4901 decreases d irectly emitted PM2.5, as we ll as carbon monoxide, formaldehyde, sulfur di oxide, irritant gases, and kno wn and suspected carcinogens, such as polycyclic a romatic hydrocarbons (PAH). I n 2008, the Central Valley Health Policy In stitute 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 Part iculate Matter: Final Report. Washington, D.C.: EPA/ 600/R-08/139F. Available at http://cfpub.epa.gov/ncea/isa/ recordisplay.cfm?deid=216546San Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-6 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard by about 13% in Bakersfield and Fr esno, resulting in an estimat ed 59 to 121 avoided cases of annual premature mortality. 7

Even though the 2008 PM2.5 Plan was developed per EPA r equirements for the 1997 PM2.5 standard (wit h a 24-hour standard o f 65 μg/m3), the 2008 plan
included a commitment to amend R ule 4901 in 2009 (with implemen tation in 2010) to align the wood-burning cu rtailment threshold with the newer 2006 PM2.5 standard (with a 24-hour standard of 35 μg/m3). Then, ba sed on research reiterating the effectiveness of Rule 4901 in protecting public health, as well as public support for a stronger rul e, the District amended and im plemented Rule 4901 in 2008—one year ahead of t he scheduled rule development a nd two years ahead of scheduled implementati on. The amended rule also set t he curtailment
level lower than init ially planned (to 30 μg/ m3) to provide an extra margin of safety and to address air qualit y forecast uncertainties.

Similarly, the District’s 2012 PM2.5 Plan committed to amend the District Rule 4901 in 2016 with compli ance beginning the winter season of 201 6-2017 with an estimated 1.5 tons per day (t pd) of PM2.5 emissi on reductions. When the District Governing Board adopted the 2012 PM2.5 Plan, guided by the HRRS

, they
directed the District to amend Ru le 4901 in 2014. As a result, the District’s
residential wood burni ng program was amended in September 2014 with implementation in the winter season of 2014-2015, two years ahe ad of the SIP
commitment. The rule was furthe r strengthened and the curtailm ent threshold lowered to 20 μg/m 3 . The combination of the lowe red curtailment threshold, tiered curtailments, increased public outreach and education, a nd increased
incentive amounts and allocations result in a much greater esti mated reduction of directly emitted PM2.5 emissions during the winter season than the previously estimated amount of 1.5 tpd.

The significant increase in t he number of curtailment days resu lting from the
lower threshold has resulted in a parallel reduction in nightti me neighborhood exposure to PM 0.1, i ncluding exposure that has been shown to o ccur as a result of indoor infiltration. This aspec t of Rule 4901, i.e. reducin g the frequency of elevated exposure to PM0.1 that induces immune system sensitiza tion and cardiovascular inflammation, has been carried forward into the HRRS. The District’s prioritization of R ule 4901 is one of the best examp les of a District policy aimed at maximizing public hea lth 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 Vall ey Health Policy Institute for the San Joaquin Valley Air Pollution Control District.
Retrieved from http://www.fresnostate.edu/chhs/cvhpi/documents/wood-burning-re port.pdfSan Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-7 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard  District grant programs reach beyond the current CAA NAAQS-SIP process to
reduce emissions in advance o f or beyond regulations. For exam ple, through the District’s popular Clean-Green-Ya rd-Machine grant program, the District has replaced close to 4,000 high-po lluting gas-powered lawn mowers with clean electric mowers, and through the Burn Cleaner Incentive Program , the District has replaced over 6,000 high-poll uting wood bur ning devices wit h cleaner alternatives. These grant program s result in a decrease in urb an, localized
health risks associated with t he use of gas-powered equipment a nd wood burning devices.

 The District’s information and educational programs, such as th e RealTime Air Quality Advisory Network (RAAN), also contribute to the HRRS.
RAAN uses real-time data from a ir monitoring stations throughou t the Valley to provide hour-by-hour air qualit y updates to schools and other s ubscribers.
Subscribers can use this info rmation to make informed decisions and plan
outdoor activities for times wit h the best air quality, reducin g potential air quality health risks. Reflecting the late st science on PM2.5 exposure risk for sensitive individuals, ambient concentration s of PM2.5 that are used to t rigger RAAN health risk warnings are more he alth 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 Vall ey population. In 2010–2011, the District sponsored the first major epidemio logical investigation of heal th effects of air pollution in the Valley, focusi ng on the populations of Modesto , Fresno, and
Bakersfield. 8 The study found that daily expos ure to high PM2.5 concentrati ons was significantly correlated with increased da ily hospital and emergency room admission rates for asthma and ot her respiratory and cardiovasc ular diseases. In 2012, the District sponsored a fo llow-up epidemiological stu dy to examine which of the chemical species fou nd in Valley PM2.5 are most hi ghly correlated with elevated ER and hospital admission rates. Results are exp ected 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 investigate d the quantity and spatial distribution of PM 0.1 plumes from motor vehicles, lawn care equipment, wood burning, and rest aurants. Currently the District is fundi ng a UC Davis research project to develop a mo del of PM0.1 population exposur e in the Valley based on previous Valley observa tional research. PM0.1 exposur e will be correlated with short- and long- term health effects by making u se of the large body of Valley epidemiological dat a that has been generated by the previous
studies described above. The Dis trict will continue to seek ou t and fund research opportunities that further the understanding of PM-related impa cts 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 Heal th Policy Institute for the Sa n Joaquin Valley Air Pollution Contro l District. Retrieved from http://www.fresnostate.edu/chhs /cvhpi/publications/index.htmlSan Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-8 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard 3.4 FIVE-FACTOR EXPOSURE ASSESSMENT METHODOLOGY

To qualitatively evaluate the pot ential risk reduction benefits from various sources, the HRRS is implemented in air quality attainment plans employing a scientifically based exposure characterization methodol ogy that draws on the latest scientific understanding about health risk from PM2.5 exposure.

The District uses a five-facto r 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 assessm ent employed is different than a formal risk
assessment. Risk assessment re quires the quantification of key elements relating to emission levels, particle or chem ical toxicity, dose-response r elationships, and total population exposure. The primar y drawback for formal risk asse ssment models in a SIP context is pervasive empirical uncertainty regarding the values of the different elements
listed above. Even if the chem ical composition, geographic pat tern 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 f rom that source because many other sources are also cont ributing to PM2.5 exposure. In addition, PM2.5 aerosols undergo photochemical aging over time and space, often resulting in new secondary organic and inorganic s pecies generated by variable r egional source loads and meteorological conditions. D espite these limitations, it i s possible to use a simple but robust exposure characteriza tion tool for making important qualitative and categorical distinctions regardi ng the relative contribution an d associated of a given source to population exposure.

3.4.1 Relevance t o Attainment

An important element of the HRRS i s the relevance of the emissi ons reductions to the Valley’s attainment of EPA’s health-based standards. This port ion of the analysis considers emissions type (such as PM2.5, NOx, or SOx), seasonal ity of the emissions, and the percent contribution of t hat source’s emissions relativ e to the Valley’s total emissions inventory. For exampl e, NOx is the limiting factor f or ammonium nitrate and
therefore reductions of NOx emissi ons in the Valley will provid e a greater impact to achieving attainment than r eductions of ammonia emissions.

3.4.2 Toxicity of Chemical Species

PM2.5 particles vary in their to xicity depending on their chemi cal composition. PM2.5 particles are characterized by a widely diverse combination of chemicals depending on unique regional combinations o f meteorology, topography, and po llution sources. In addition to experimental and clin ical research that has identif ied these toxicity differences, epidemiological studi es have found regional differ ences in health impactsSan Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-9 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard despite comparable region al PM2.5 mass exposure. 9 Beyond the intrinsic toxicity of individual chemicals, the uniqu e combinations of chemicals gene rated by some sources can actually magnify health ri sk above and beyond what their ma ss concentrations would suggest. 10

Many emissions sources evaluated i n this plan are sources of di rect (primary) PM2.5 emissions characterized by a uni que combination of chemical spe cies. Other sources emit chemical species such as ammonia and nitrogen oxides (NOx) , precursors that
contribute to the formation o f secondary PM2.5 species. The PM 2.5 chemical species categories adopted in the exposure characterization model inclu de elemental carbon (carbon black), organic carbon co mpounds (OC), metals (elements ), ammonium nitrate, ammonium sulfate, and geological . PM2.5 is regularly speciated at several Valley monitoring sites. The following discussion provides an overvie w of PM2.5 species and their associated health impacts.

Organic carbon (OC): OC species found in PM2.5 aeros ol are generated as primary organic aerosol (POA), predominant ly through the combustion of hydrocarbons. Key POA sources include cooking, in dustrial processes, mobile sourc e exhaust, prescribed burning, tire wear, and wood burning. 11 Secondary organic aerosol s (SOA) are formed
from the oxidation of motor v ehicle hydrocarbons, prescribed bu rning, wood burning, solvent use, and industrial processes.

OC is recognized as one of the mo st biologically reactive of PM 2.5 chemical species categories, with ample evidence of high toxicity found in exper imental, clinical, and epidemiological studies. OC, often in combination with metals such as iron, has been shown to generate reactive oxygen species (ROS) that drive seve ral different mechanisms of pulmonary inflamma tion, including disruption of n ormal immune system functioning. 12 In addition, OC and metals have been shown to indirectly stim ulate ROS production by macrophages, which are cells responsible for defe nding the lungs from pathogens and aerosols.

One of the primary OC species ca tegories is polycyclic aromatic hydrocarbons (PAH). PAH species fall into two categorie s: a high molecular weight f raction and a low molecular weight fraction. The former is found in diesel exhau st 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 In stitute. 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/cont ent/60/8/612.full doi:
doi:10.1136/oem.60.8.612

11 U.S. Environmental Protectio n 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 Particulat e Matter and Nanoparticles by Me asuring Oxidative Stre ss Potential—A Workshop Report and Consensus Statement. Inhalation Toxicology 20, 75–99. Retrieved from http://faculty.unlv.edu/buckb/scann ed%20pfd/Ayres% 20et%20al%202 008.pdf

13 Landvik, N.E., Gorria, M., Arlt, V.M., Asare, N., Solhaug, A., Lagadic-Gossmann, D., & H olme, J.A. (2007). Effects of Nitrated-Polycyclic Aromati c Hydrocarbons and Diesel Exhaust Particle Extracts on Cell Signalling Related toSan Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-10 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard hydrocarbon combustion particles and serves as a precursor to t he formation of an important OC species category known as quinones. Formed from a tmospheric processing of PAH or within the body (in vivo), quinones have b een shown to be one of the most important drivers of pulmonary oxidative stress, resul ting 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 pat ients in Fresno found that quino ne levels in urine correlated with sustained (multi- day) high ambient concentratio ns 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 c ooking (especially charbroiling). Compared to OC s pecies, there is limited eviden ce of comparable impacts on ROS production, pulm onary inflammation, and immune s ystem disruption. For example, EC appears not to be a significant agent for the i nduction of inflammation in macrophage cells, indicating a s ignificantly lower toxicity level relative to OC species. 16 A recent study of PM 0.1-based ex posure of EC in mice found m odest
cardiovascular effects. Pulm onary inflammation was noted but o nly at high doses beyond normal ambient concentrations. 17 A recent study in Mexico City found an association between exposure le vels of EC and lung function dec rements among
asthmatic and non-asthmatic children. 18

Characterization of health effect s of elemental carbon from hum an exposure studies is complicated by the high correla tion between EC, OC, and metals emitted by diesel exhaust. Exposure to EC is a P M2.5 risk factor, although there is more evidence to date that other chemical specie s, e.g. metals and OC, found in these particles are the primary drivers of neg ative health effects.

Metals: A combination of clinical, exper imental, and epidemiological st udies have implicated several of the meta ls found in PM2.5 with negative r espiratory or cardiovascular outcomes, somet imes in conjunction with the acti on of OC species. One of the most important is iron bec ause of its ability to catalyz e the production of hydrogen peroxide, leading to highly reacti ve hydroxyl radicals (OH). I n turn, these highly reactive chemicals stimulate the producti on and action of cytokines by m acrophages. Cytokines

Apoptosis:Possible Implications fo r their mutagenic and Carcino genic Effects. Toxicology, 231, 159–174.
doi:10.1016/J.tox.2006.12.009

14 Bolton, J., Trush, M.A., Penni ng, T.M., Dryhu rst, 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., Ty ner, T.R., Krishnan, V.V., & Hasson, A.L. (2012). An Inve stigation o f the Use of Urinary Quinones as Environmental Biomarkers for Exposure to Am bient Particle-Borne Pollutants. Science of the
Total Environment (submitted).

16 Vogel, C.F., Sciullo, E., Wong , P., Kuzmicky, P., Kado, N. & M atsumura, F. (2005). Inducti on of Proinflammatory Cytokines and C-Reactive Protein in Human Macrophage Cell Line U937 Exposed to Air Po llution 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 Bla ck Nanoparticles and Vascular E ffects. Particle and Fibre Toxicology 7:33

. Retrieved from http://www.particleandfibretoxi cology.com/con tent/7/1/33 doi: 10.1186/1743-8977-7-33

18 Barraza-Villarreal, A., Escam illa-Nuñez M.C., H ernández-Cadena L., Texcalac-Sangrador. J.L., Sienra-Monge, J.J., Del Río-Nava rro, 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.San Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-11 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard are cell-signaling mole cules that are criti cal to normal functi oning of the immune system. A recent experimental study e xamined the impact of iron in sili ca particles in triggering respiratory toxicity. 19 Compared to silica particles wit h no iron, silica particles w ith iron were found to have a significantly greater effect on oxidative stress via hydrogen peroxide production with subsequent stimulus of cytokines by ma crophages.

Extensive research relates expos ure in metals (particularly nic kel and vanadium) in
PM2.5 to cardiovascular effect s. A national epi demiological st udy recently found that communities with higher fracti ons of nickel, vanadium, and EC i n their PM2.5 also had higher risk of cardiovascular and respiratory hospitalization. 20 Specifically, cardiovascular hospitalizations were 26% higher in counties wit h a nickel fraction in the
75 th percentile versus counties with nickel in the 25% percentile. In an investigation of the relatively higher associati on between PM2.5 daily concentra tions and daily rates of cardiovascular mortality in New York City, the exceptionally hi gh level of nickel and vanadium resulting from residual oil fly ash used for heating a nd as fuel for ships were identified as a principle c ardiovascular risk factor. 21 In a related study, rats exposed to PM2.5 with high fractions of chrom ium, iron, and nickel fractio ns responded with significantly reduced heart rate va riability and increased hear t rates, each being an indicator of cardiovascular disruption and risk. 22

In conclusion, metals found in P M2.5 produced from combustion o f coal, residual oil, diesel fuel, and motor oil are re cognized as chemical drivers o f cardiovascular and respiratory morbidity and morta lity. This has led some researc hers to conclude that regional differences in U.S. car diovascular mortality that cann ot 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 inorgan ic species (not directly emitted) primary source of PM2.5, and it does not contain carbon. Nitrate is formed by atmospheric reactions between two precurso rs: ammonia and nitric acid. Prior to this reaction, n itric acid generally originates from the chemical processing of nitrogen oxides (NOx), largel y from fuel combustion during m ultiday stagnation events. As seen in the following figure, nitrate is significan t 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., Leppe rt, V.J. & Forman, H.J. (2011). Iron-Mediated Lipid Peroxidation and Lipid Ra ft Disruption in Low-Dose Silica -Induced Macrophage Cytokine Production. Free Radical Biology and Medicine, 51(6) , 1184–1194. doi: 10.1016/j.fr eeradbiomed.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/cont ent/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 Am bient Air Particulate Ma tter (PM) on Human Health. Inhalation Toxicology, 21(1), 1–31. Retrieved from http://faculty.unlv.edu/buckb/sc anned%20pfd/Chen %20and%20Lippma nn%202009.pdf

23 Lippman, M. (2012, April 16). Presentation: Results from Natio nal Particle Component Toxicity (NPACT) Program and NYU: Toxicology Findings, Int egration, and implications. Pr esented at the Annual Meeti ng of the Health Effects Institute (HEI) in Chicago, IL, A pril 15–17, 2012 . Presentation retrieved from http://www.healtheffects.org/Slides/AnnConf2012/Lippmann-MonPM. pdfSan Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-12 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard 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 nitr ate is very low, with an LD50 (dose causing death for 50 % of the exposed subjects) repor ted to be two thirds
that of table salt. This rais es the question as to whether oth er factors intrinsic to
inhalation could lead to health e ffects at considerably lower e xposure concentrations. As seen in the case of OC species, the most compelling evidence of species toxicity is built on a foundation of experim ental, clinical, and epidemiolo gical research. In particular, epidemiological studi es draw their inferences from statistical associations between exposure variables and heal th outcomes only. Uncoverin g the actual mechanisms of harm, therefore, r equires further isolation of me chanisms through experimental and cl inical research.

In the case of ammonium nitrate , evidence of toxicity is largel y limited to epidemiological research alone. For example, a r ecent epidemiological study of traffic air toxics and pre-term birth in Los Angeles fou nd statistical associations be tween nitrate mass, PAH, and several other air pollutants and the increas ed likelihood o f pre-term birth. 24 The authors point to other experiment al studies that identified ver y high oxidative stress potential resulting from PAHs, m etals, and other OC species col lected from Los Angeles traffic sources as being the li kely mechanism for pre-term birt h. They conclude by emphasizing the need to further st udy the links between pre-ter m birth and PAH

exposure.

24 Wilhelm, M., Ghosh, J.K., Su, J ., Cockburn, M., Jerrett, M. & Ritz, B. (2011). Traffic-Rela ted Air Toxics and Preterm Birth: A Population-Based Case-Control Study in Los Angeles Cou nty, California. Environmental Health 10: 89

. Available at http://www.ehjournal.net/content/10/1/89/ doi: 10.1186/1476-069X-10-89San Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-13 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard One experimental study was found that explicitly looked for tox ic mechanisms driven by
ammonium nitrate. 25 The study exposed rats to hi gh concentrations of nitrate (70 to 420 μg/m 3 ) in combination with EC. After exposure, animals were sacrifi ced and a necropsy was performed, followed by a r ange of tests for pathological im pacts between the control (non-exposed) and expos ed groups. The authors did not find abnormalities that could be tied to the experimental e xposure to nitrate alone or in combination with EC. This absence of experimental evi dence for mechanisms of patholo gy for inhaled
ammonium nitrate is consisten t with its low oral toxicity.

Ammonium sulfate : Ammonium sulfate (sulfate) i s also classified as a secondary inorganic species. It is formed w hen sulfuric acid, itself a p roduct of oxidation of sulfur,
reacts with ammonia. Mass conc entrations of sulfate are signif icantly 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 co ncentrations of sulfate are not appreciably differ ent in cold and hot seasons.

Research findings regarding the to xicity of sulfate are compara ble to that of nitrate. Oral toxicity is low and it i s approved as a food additive by t he US Food and Drug Administration and the European Union. One study 26 examined the response of 20 non-smoking subjects to four-hour exposure sessions in chambers containing 500 μg/m 3 of sulfate aerosol, a concentrati on over two orders of magnitu de above ambient levels in the Valley. Pulmonary function tests were performed to assess the response of these exposures. No significant changes in pulmonary functi on or bronchial reactivity were observed immediately after the individual exposures or 24 hours after exposure. In an experimental study that a lso exposed rats to 500 μg/m 3 of sulfate for four to eight months, modest pulmonar y impacts were noted. 27 After four months, cellular immunologic responsiveness was not i mpaired, but physiologic ch anges were detected, including enlargement of bronchi al epithelial (surface) cells a nd in alveolar size.

For each of these studies, the mo dest health impacts observed a t very high exposure levels are consistent with the low intrinsic toxicity of sulfat e. This is consistent with results of a review of the epidem iological and toxicological re search on sulfate. 28

Researchers found that PM sulfat e was a weaker indicator of hea lth risk than PM2.5
mass. Because sulfate is correla ted with PM2.5 mass, this resu lt is inconsistent with sulfate having a strong health influence. The study concluded that the epidemiologic

25 Cassee, F., Arts, J .H., Fokkens, P.H., S poor, S.M., Boere, A.J ., van Bree, L., & Dormans, J.A. (2002). Pulmonary
Effects of Ultrafine and Fine A mmonium Salts Aerosols in Health y and Monocrotaline-Treated Rats Following ShortTerm Exposure. Inhalation Toxicology, 14(12) , 1215–1229. doi: 10.1 080/08958370290084872

26 Kulle, T.J., Sauder, L.R., Shant y, F., Kerr, H.D., Ferrell, B. P., Miller, W.R., & Milman, J.H. (1984). Sulfur Dioxide
and Ammonium Sulfate Effects on Pu lmonary Function and Bronchia l Reactivity in Human Subjects. American Industrial Hygiene Association Journal, 45(3) , 156–161. ISSN: 1542-8125

27 Smith, L.G., Bu sch, R.H., Buschbom, R.L ., Cannon, W.C., Loscut off, S.M., & Morris, J.E. ( 1989). Effects of Sulfur Dioxide or Ammonium Sulfate Expos ure, 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., Cro ss, C.E., Hidy , G., Hoel, D., Mc Clellan, R., Moolgavkar, S. (2007). Evidence of Health Impacts of Sulfate-and Nit rate-Containing Particles in A mbient Air. Inhalation Toxicology, 19(5), 419-449.
doi:10.1080/08958370601174941San Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-14 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard and toxicologic evidence provi de little or no support for a cau sal association of sulfate
and health risk at ambient concentrations.

Geological: Winter season and annual average PM2.5 found in the Valley cont ains a very small fraction of species that are termed crustal , i.e. having their origins in the
earth’s crust. This coarse frac tion—PM 2.5-10—contains a much higher fraction, as do particles beyond the PM10 size category. Suspended dust consis ts mainly of oxides of aluminum, silicon, calcium, titani um, iron, and other metal oxi des. The precise
combination of these com ponents depends on the geology, industr ial, and agricultural processes of the area. Geological material typically consists of 5% to 15% PM particles.

Other researchers examined the re spiratory inflammation potenti al of PM2.5 soil dust
from windblown dust and vehicl e-generated particles from unpave d roads, taken from
nine different sites i n the western U.S. 29 None of the sites were located in the Valley. Cultured human epithe lial cells were expos ed and then were asse ssed for their release of cytokines known to be trigger ed 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 co ntributing factor to the variations in inflammatory potential.

Although not technically a geolog ic species, respirable road du st (RRD) has been recognized and analyzed as a separat e form of PM2.5 that has re levance to exposure
characterization. In this cont ext, RRD is defined as PM less t han 2.5 microns in diameter that is deposited along pa ved roadways as a result of roadway breakdown, tire wear, brake wear, deposition of e xhaust-related particles, and other anthropogenic sources. Speciation analysis 30 of RRD in southern California identified over 100 organic compounds including n-alkanes, n -alkanoic acids, n-alkenoic aci ds, n-alkanals, nalkanols, benzoic acids, benzalde hydes, polyalkylene glycol eth ers, 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 associat ed with motor vehicle exhaust and component wear. RRD particles are re-suspended by passing traffic, leaf blowers, and other sources for po ssible inhalation by individua ls 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 ma ss and, by itself, has relative ly 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., Ver anth, M.M., Moss, T.A., Langelie r, C.R., Lanza, D.L., & Yos t, G.S. (2004). Inflammatory Cytokines and Cell Death in BEAS- 2B Lung Cells Treated with Soi l Dust, Lipopolysaccharide , and Surface-Modified
Particles. Toxicological Science 82(1) , 88–96. Retrieved from http://toxsci.oxfordj ournals.org/content/82/1/88.full.pdf+html doi: 10.1093/toxsci/kfh24

30 Rogge, W. F., Hildemann, L. M., Maz urek, M. A., C ass, G. R. an d Simoneit, B. R. T. (1993). Sources of Fine Organic Aerosol—3. Road Dust, Tire Debris, and Organometallic B rake Lining Dust—Roads As Sources and Sinks. Environmental Science & Technology 27(9), 1892-1904.San Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-15 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard 3.4.3 Particle Siz e and Deposition

Particle size has a signific ant bearing on bod ily deposition, n et exposure, and corresponding health risk, even wit hin the PM2.5 size fraction. Key metrics for deposition assessment include t he percentage of inhaled particl es that remain deposited and not exhaled (known a s the deposition fraction) an d 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 gr eater than 10 microns are least likely to be exhaled, and thus have higher deposition fractions. 32

The relationship between parti cle 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 th e respiratory tract is the primary zone of deposition for the sm allest and largest particles. Approximately 80% of extremely small particles of one nanometer (0.001 micron)
diameter or less are retained her e with a compar able deposition fraction in the 10
micron diameter.

 Tracheobronchial: The deposition fraction in this z one peaks at nearly 40% for particles with diameters bet ween 1 and 10 nanometers. Almost 1 00% 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 dis sipation of deposition beyond the PM 0.1 size.

31 International Commission on Radi ological Protection [ICRP]. (1 995). Human Respiratory Tract Model for Radiological Protection . ICRP Publication 66.. Annals of the ICRP 24, 1–3.

32 U.S. Environmental Protectio n 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=87903San Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-16 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard Figure 3-3 Relationships between P article Size Distribution and Respiratory Deposition Zones

Deposition of very small particl es in the alveolar region of th e lungs results in the delivery of their chemicals into the bloodstream where they pro mote cardiovascular disruption and immune system sensitization. 33 These chemicals can trigger heart attacks and premature death among individual s with pre-existing heart conditions. 34 Extremely small particles can al so be absorbed into the brain v ia the nasal tract, bypassing the protection provid ed by the blood-brain barrier. 35 The effects of particles deposited primarily in the trac heobronchial region center on re spiratory function. 36

33 Delfino, R.J., Siout as, C., & Malik, S. (2005). Potential Role of Ultrafine Particles in A ssociations between Airborne
Particle Mass and Cardiovascular Health. Environmental Health Perspectives 113(8), 934–946. Retrieved from http://ehp03.niehs.nih.gov/article /fetchArticle.action?articleU RI=info%3Adoi%2F10.1289%2Fehp.7938

34 Nel A. (2005). Air Pollution-Rela ted Illness: Effects of Parti cles. 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=216546San Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-17 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard As depicted in Figure 3-4, par ticle deposition and associated h ealth risk is magnified by exercise in several ways. Fir st, the amount of inhaled air per minute rises substantially when breathing faster and more deeply. Second, breathing harde r means that particles, especially PM 0.1, are more like ly to penetrate the alveolar re gion of the lungs where absorption into the bloodstream occurs. A 2003 study 37 found that during moderate
exercise 80% of inhaled PM 0.1 was deposited in the lungs, comp ared with 60% lung retention while at rest (see le ft panel in Figure 3-4). Howeve r, because the volume of air exchanged per minut e increases substant ially during exercis e, overall PM 0.1 deposition increased by 450% (ri ght panel). This phenomenon un derscores the health risk posed to individuals who work or exercise in areas where s ources of hydrocarbon combustion result in very high PM 0.1 particle concentrations.

Figure 3-4 Particle Number De position Fraction (DF) and Total Particle Deposition of PM0.1 at Rest and Exercise

3.4.4 Exposure to Ultrafi ne Particles (PM 0.1)

Elevated exposure to freshly emi tted PM 0.1 is a critical healt h risk factor that often does not correspond to ambient P M2.5 concentrations at local mo nitors. PM 0.1 are formed through nucleation and gas- to-particle reactions and gro w (or shrink) through a number of mechanisms including condensation, coagulation, and v olatilization. 38 High concentrations of primary (direct ly emitted) PM 0.1 are typical ly found near fresh sources of hydrocarbon combusti on, including coal plants, charb roiled meat, diesel and gasoline vehicles, wood combus tion, and lawn care equipment. T hese combustion

37 Daigle, C., Chalupa, D.C., Gi bb, F.R., Morrow, P.E., Oberdörst er, G., Utell, M.J., & Frampton, M.W. (2003). Ultrafine Particle Deposition in Humans during Rest and Exercis e. Inhalation Toxicology, 15(6) , 539–552. doi:
10.1080/08958370304468

38 Solomon, P. (2012). An Overview o f Ultrafine Particles in Ambi ent Air. EM: Journal of the Air & Waste Management Association, May, 18–26.San Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-18 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard particles start out very small, g row larger over time and space , and evolve chemically at the same time. Secondary PM 0.1 typically is formed via partic le nucleation from gas or liquids and is characterized by larger geographic scales and mo re uniform population

exposure.

Despite being extremel y small, PM 0.1 has an extremely high sur face area, as seen in Figure 3-5. Compared to an equal m ass of particles of two micr ons (PM 2.0) in diameter, ultrafine particles tha t are 1,000 times smaller (20 nanometers or PM 0.02)
nonetheless have 125 time s the surface area. 39 In addition, PM 0.1 produced by hydrocarbon combustion typically contain a rich mixture of chem icals with potential health effects, including nicke l, iron, vanadium, PAH, and othe rs. 40 Chemical potency, very high surface area, and alv eolar deposition ar e signal char acteristics of PM 0.1 from hydrocarbon combustion that res ult in significant health risks from chronic exposure.

Figure 3-5 Electron Microgra ph of an Ultrafine Particle 41

Sub-populations who live or work near sources of primary PM 0.1 from hydrocarbon combustion are particularly a t risk. Health scientists have ge nerated an overwhelming body of epidemiological (statist ical) evidence that individuals near freeways (less than 300 meters) are being harmed via ch ronic inhalation of PM 0.1 f rom vehicles. 42 Similarly, a 2011 study of resident ial wood burning in Cambria, California found very high neighborhood concent rations of PM 0.1 from wood smoke even though
concentrations of PM2.5 at the nearby ambient monitor met the f ederal health

39 Donaldson, K., Stone, V., Clout er, 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., & J ayaratne, E.R. (2008). Ambient Nano and Ultrafine Particles from Motor Vehicle Emissions: Characteristics, Ambie nt 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-Rela ted Illness: Effects of Parti cles. Science, 308(5723), 804–806. doi:
10.1126/science.1108752

42 Gauderman, W., Vora, H., McCon nell, 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_upsellSan Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-19 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard standard. 43 The health risk from fresh sour ces of PM 0.1 has important en vironmental justice implications to the ext ent that elevated exposure to ne ar-source PM 0.1 is
concentrated in communities tha t already face sources of risk r elated to race or
socioeconomic status. 44 Chronic exposure to near-sour ce PM 0.1 commonly occurs in
locations where local monitors a re in attainment for PM2.5 stan dards and during
seasons when ambient PM2.5 conc entrations are below the annual daily standard.

3.4.5 Population Proximity and Intake Fraction

Estimating total exposure and ne t health risk from a given sour ce of PM2.5 requires that population proximity and population density be considered in ad dition to the source’s
contribution to the r egional PM2.5 emission s inventory and its toxicity. In addition to factors governing net deposition of inhaled particles reviewed above, net population exposure from the source in ques tion is also shaped by the numb er of exposed
individuals who inhale the emissi ons and the duration of exposu re in conjunction with aerosol concentration levels (s ee Figure 3-6). Known as the in take fraction, this measure of population exposure is defined empirically as the po llutant mass inhaled divided by the mass emitted. 45 Intake fraction is useful in connecting emissions to
health risk because the mass inhal ed is a better indicator of h ealth risk than the mass
emitted or airborne co ncentration. Two different pollutant sou rces with very comparable emission rates of the same po llutant can nonetheless have signi ficantly different intake fractions depending on the surroundi ng population density. For example, sources of
PM2.5 located in rural areas m ay have an intake fraction that i s 10 to 100 times smaller than a comparable sour ce located within a d ensely populated cit y.

Figure 3-6 Simplified Intake Fraction Model

The relevance of the intake fr action concept can be seen in a r ecent study of neighborhood variabilit y in wood smoke concentrations in Cambri a, California. 46 The

43 Thatcher, T. & Kirchstetter, T. (2011). Assessing Near-Field Exposures from Distributed Residential Wood Smoke
Combustion Sources . Report prepared for the Californi a Air Resources Board. Retri eved from http://www.arb.ca.gov/researc h/rsc/10-28-11/it em2dfr07-308.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 Calif ornia, Davis, Center for Region al Change. Retrieved from http://regionalchange.ucdavis.edu/ publications/R eport_Land_of_R isk_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 Califor nia Air Resource s Board Report.

46 Thatcher, T. & Kirchstetter, T. (2011). Assessing Near-Field Exposures from Distributed Residential Wood Smoke
Combustion Sources . Report prepared for the Californi a Air Resources Board. Retri eved from http://www.arb.ca.gov/researc h/rsc/10-28-11/it em2dfr07-308.pdfSan Joaquin Valley Unified Air Polluti on Control District April 16, 2015

3-20 Chapter 3: Health Impacts and the Health Risk Reduction Strategy
2015 Plan for the 1997 PM2.5 Standard winter study found very high conc entrations of PM 0.1 on a neig hborhood scale that
were often not reflected in PM2. 5 concentrations measured by lo cal air quality monitors. In effect, a single wood-burning household had the effect of en veloping the adjacent
and downwind homes with a PM 0.1 plume. Furthermore, the study also found that
wood smoke PM 0.1 was infiltra ting adjacent homes that were not burning, with an average indoor concentration found to be 74% as high as immedia tely outside the homes. Taking into consideration the length of PM 0.1 inhalati on during sleeping hours, the relatively high concentrati on of PM 0.1 found in the plume, and the number affected of individuals in an urban neigh borhood, the intake fraction re sulting from the source of the wood smoke would be very hi gh. Assuming that this nightly exposure occurred over the course of a season, the cumu lative health risk to the neigh borhood would be
considerable and would almost cer tainly exceed the risk indicat ed by daily
concentrations of PM2.5 measur ed by ambient monitors.

3.5 HEALTH BENEFITS ACHIEVED B Y REDUCING PM2.5 EMISSIONS

Understanding the results of any HRRS strategy is critical to a ssessing the overall value and success of that strategy. Over the course of the past deca de, ongoing progress in the fields of epidemiology and geographic information systems ( GIS) have resulted in the development of computer model s that are capable of estimati ng the health benefits of improved air quality with r easonable accuracy when properly applied. These models
estimate the number of avoided ca ses of certain diseases and ot her health impairment categories, known as health end points, which result from a spec ified reduction in exposure to criteria air pollutants.

EPA developed a sophisticated com puter software model called Be nMAP that is wellsuited for estimating health benef its and that can therefore be employed in order to
estimate the annual reductions in morbidity (disease) and morta lity (premature death) attributable to improved air quality due. As the District cont inues to develop air quality attainment plans in future year s to address the increasingly st ringent NAAQS, the
District will evaluate health benef its for Valley residents res ulting from adopted air quality attainment plans.