Appendix F

Non-Cancer Health Risk
F - 1

Non-Cancer Health Risk

I. Health Impacts Assessment

A substantial number of epidemiologic studies have found a strong association 

between exposure to ambient PM2.5 and a number of adverse health effects

(ARB, 2002). For this report, ARB staff quantified seven non-cancer health 

impacts associated with the change in exposures to the diesel PM emissions. 

Staff estimates that approximately 90 premature deaths (30 – 160, 95 percent 

confidence interval (95% CI)) are associated with the baseline uncontrolled 

emissions from commercial harbor craft in the year 2004. Other health impacts 

are listed in the Table 1. The methodology for estimating these health impacts is 

outlined below. Details can be found in Appendix A of the Emission Reduction 

Plan for Ports and Goods Movement in California (ARB, 2006).

Table 1: Baseline Health Effects Associated With

Commercial Harbor Craft Emissions

for the year 2004*

Endpoint Pollutant

# of Cases

95% CI

(Low)

# of Cases

(Mean)

# of Cases

95% CI

(High)

PM 10 50 80

Premature Death NOx 10 50 80

Total 30 90 160

PM 10 10 10

NOx 10 10 10

Hospital 

admissions 

(Respiratory) Total 10 20 30

PM 10 20 30

NOx 10 20 30

Hospital 

admissions 

(Cardiovascular) Total 20 40 60

PM 450 1,200 1,900

NOx 490 1,200 2,000

Asthma & Lower 

Respiratory 

Symptoms Total 940 2,400 3,900

PM 0 100 210

Acute Bronchitis NOx 0 100 220

Total 0 200 430

PM 6,600 7,800 9,000

Work Loss Days NOx 6,600 7,800 9,000

Total 13,000 16,000 18,000

PM 37,000 45,000 54,000

NOx 37,000 45,000 53,000 Minor Restricted 

Activity Days

Total 74,000 90,000 110,000

* Health effects from primary and secondary PM are labeled PM and NOx, respectively. The sum 

of PM and NOx impacts may not equal the total given due to rounding.
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Since diesel PM is a constituent of ambient PM2.5, using the epidemiologic study 

results to quantify diesel PM health effects is reasonable. This analysis shows 

that the statewide cumulative impacts of the emissions reduced through this 

regulation from year 2009 through 2025 are approximately:

• 310 premature deaths (90 – 530, 95% CI)

• 70 hospital admissions due to respiratory causes (40 – 90, 95% CI) 

• 120 hospital admissions due to cardiovascular causes (80 – 190, 95% CI)

• 8,100 cases of asthma-related and other lower respiratory symptoms 

(3,100 – 13,000, 95% CI)

• 670 cases of acute bronchitis (0 – 1,500, 95% CI)

• 53,000 work loss days (45,000 to 61,000, 95% CI)

• 300,000 minor restricted activity days (250,000 to 360,000, 95% CI)

Table 2 lists the impacts associated with primary and secondary diesel emissions 

separately. Details can be found in Appendix A of the Emission Reduction Plan 

for Ports and Goods Movement in California (ARB, 2006).

Table 2: Total Health Benefits Associated with Reductions in Emissions

from Commercial Harbor Craft

(2009-2025)*

Endpoint Pollutant

# of Cases

95% CI

(Low)

# of Cases

(Mean)

# of Cases

95% CI

(High)

PM 50 200 340

Premature Death NOx 30 110 190

Total 90 310 530

PM 30 40 60

NOx 20 20 30

Hospital 

admissions 

(Respirat ory) Total 40 70 90

PM 50 80 120

NOx 30 40 70

Hospital 

admissions 

(Cardiovascular) Total 80 120 190

PM 1,900 5,000 8,100

NOx 1,200 3,100 4,900

Asthma & Lower 

Respiratory 

Symptoms Total 3,100 8,100 13,000

PM 0 420 920

Acute Bronchitis NOx 0 250 540

Total 0 670 1,500

PM 28,000 34,000 39,000

Work Loss Days NOx 16,000 19,000 22,000

Total 45,000 53,000 61,000

PM 160,000 190,000 230,000

NOx 91,000 110,000 130,000 Minor Restricted 

Activity Days

Total 250,000 300,000 360,000

* Health effects from primary and secondary PM are labeled PM and NOx, respectively. The sum 

of PM and NOx impacts may not equal the total given due to rounding.
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1. Primary Diesel PM 

Lloyd and Cackette (2001) estimated that, based on the study by Krewski and 

colleagues (2000) of the American Cancer Society (ACS) cohort, a statewide 

population-weighted average diesel PM2.5 exposure in year 2000 of 1.8 μg/m3

can be associated with a mean estimate of 1,985 premature deaths per year in 

California (Lloyd and Cackette, 2001). In 2002, Pope and colleagues published 

new findings with the same ACS cohort based on a longer follow-up time and 

improved statistical modeling techniques. Consistent with U.S. EPA (2004), ARB 

has been using the new PM-premature death relationship from Pope et al. (2002) 

since the approval of the Ports and Goods Movement Emission Reduction Plan 

(ARB, 2006). Using the study by Pope et al. (2002), a statewide populationweighted average diesel PM2.5 exposure of 1.8 μg/m3

 can be associated with a 

mean estimate of 2,200 premature deaths per year in California, about 10% 

higher than previous estimates. The diesel PM2.5 emissions corresponding to 

the diesel PM2.5 concentration of 1.8 μg/m3 is 36,000 tons for the year 2000 

based on the emission inventory developed for this rule. Using this information, 

we estimate that for every reduction of 17 tons per year of diesel PM2.5

emissions, one fewer premature death would result. This factor is derived by 

dividing 36,000 tons of diesel PM by 2,168 deaths (unrounded number of deaths 

described above). Although a single statewide factor (tons per death) is 

discussed in this example, staff actually developed basin-specific factors for the 

health impacts assessment of emissions from commercial harbor craft. These 

basin-specific factors were developed using basin-specific diesel PM 

concentrations and emissions for the year 2000. After adjusting for population 

changes between each future year and 2000, staff estimates that the cumulative 

total of 2,020 tons of emissions from commercial harbor craft reduced through 

the implementation of this regulation in years 2009-2025 are associated with a 

reduction of approximately 200 deaths (50 – 340, 95% CI). Estimates of other 

health benefits, such as hospitalizations and asthma symptoms, were calculated 

using basin-specific factors developed from other health studies. Details on the 

methodology used to calculate these estimates, including the adjustment for offshore PM emissions in the 3 – 24 nautical mile domain, can be found in 

Appendix A of the Emission Reduction Plan for Ports and Goods Movement in 

California (ARB, 2006).

2. Secondary Diesel PM

In addition to directly emitted PM, diesel exhaust contains NOx, which is a 

precursor to nitrates, a secondary diesel-related PM formed in the atmosphere. 

Lloyd and Cackette (2001) estimated that secondary diesel PM2.5 exposures 

from NOx emissions can lead to additional health impacts beyond those 

associated with directly emitted diesel PM2.5. To quantify such impacts, staff 

developed population-weighted nitrate concentrations for each air basin using 

data not only from the statewide routine monitoring network, which was used in 

Lloyd and Cackette (2001), but also from special monitoring programs such as 
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IMPROVE and Children’s Health Study (CHS) in year 1998. The IMPROVE 

network provided additional information in the rural areas, while the CHS added 

more data to southern California. Staff calculated the health impacts resulting 

from exposure to these concentrations of PM and then associated the impacts 

with the basin-specific NOx emissions to develop basin-specific factors (tons per 

case of health impact). Using an approach similar to that used for primary diesel 

PM and adjusting for population changes between each future year and 1998 

(the year with the greatest geographic extent of nitrate monitoring), staff 

estimates that the cumulative reduction of 36,400 tons of emissions from 

commercial harbor craft in 2009-2025 are associated with the reduction of an 

estimated 110 premature deaths (30 – 190, 95% CI). Other health effects were 

also estimated as outlined above.

Assumptions and Limitations of Health Impacts Assessment

Several assumptions were used in quantifying the health effects of PM exposure. 

They include the selection and applicability of the concentration-response 

functions, exposure assessment, and baseline incidence rates. These are briefly 

described below.

• For premature death, calculations were based on the concentrationresponse function of Pope et al. (2002). The ARB staff assumed that the 

concentration-response function for premature death in California is comparable 

to that developed by Pope and colleagues. This is supported by other studies 

(Dominici et al. 2005, Franklin et al. 2007) in California showing an association 

between PM2.5 exposure and premature death similar to that reported by Pope 

et al. (2002). In addition, the Pope et al. (2002) study included subjects in several 

metropolitan areas of California. The U.S. EPA has been using the Pope et al. 

(2002) study for its regulatory impact analyses since 2004. For other health 

endpoints, the selection of the concentration-response functions was based on 

the most recent and relevant scientific literature. Details are in the Emission 

Reduction Plan for Ports and Goods Movement in California (ARB, 2006).

• The ARB staff assumed the model-predicted diesel PM exposure 

estimates published in the report titled “Proposed Identification of Diesel Exhaust 

as a Toxic Air Contaminant” (ARB, 1998) could be applied to the entire 

population within each basin. That is, the entire population within the basin was 

assumed to be exposed uniformly to modeled concentration, an assumption 

typical of this type of assessment.

• The ARB staff assumed the baseline incidence rate for each health 

endpoint was uniform across each county, and in many cases across each basin. 

This assumption is consistent with methods used by the U.S. EPA for its 

regulatory impact assessment, and the incidence rates match those used by U.S. 

EPA.
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• Although the analysis illustrates that reduction in diesel PM exposure 

would confer health benefits to people living in California, we did not provide 

estimates for all endpoints for which there are C-R functions available. Health 

effects such as myocardial infarction (heart attack), chronic bronchitis, and onset 

of asthma were unquantified due to the potential overlap with the quantified 

effects such as lower respiratory symptoms and hospitalizations. In addition, 

estimates of the effects of PM on low birth weight and reduced lung function 

growth in children are not presented. While these endpoints are significant in an 

assessment of the public health impacts of diesel exhaust emissions, there are 

currently few published investigations on these topics, and the results of the 

available studies are not entirely consistent (ARB, 2006). In summary, because 

only a subset of the total number of health outcomes is considered here, the 

estimates should be considered an underestimate of the total public health 

impact of diesel PM exposure.

II. Economic Valuation of Health Effects

This section describes the methodology for monetizing the value of avoiding 

adverse health impacts.

The U.S. EPA has established $4.8 million in 1990 dollars at the 1990 income 

level as the mean value of avoiding one premature death (EPA, 1999). This

value is the mean estimate from five contingent valuation studies and 21 wagerisk studies. Contingent valuation and wage-risk studies examine the willingness 

to pay (or accept) for a minor decrease (or increase) in risk of premature death. 

For example, if 10,000 people are willing to pay $800 apiece for risk reduction of 

1/10,000 then collectively the willingness-to-pay for avoiding a premature death, 

in this example, would be $8 million. This is also known as the “value of a 

statistical life” or VSL.1

As real income increases, people are willing to pay more to prevent premature 

death. U.S. EPA adjusts the 1990 value of avoiding a premature death by a 

factor of 1.2012 to account for real income growth from 1990 through 2020, 

(EPA, 2004). Assuming that real income grows at a constant rate from 1990 until 

2020, we adjusted VSL for real income growth, increasing it at a rate of

approximately 0.6% per year. We also updated the value to 2006 dollars. After 

these adjustments, the value of avoiding one premature death is $8.2 million in 

2006, $8.6 million in 2015 and $9.2 million in 2025, all expressed in 2006 dollars.

 

1 U.S. EPA’s most recent regulatory impact analyses, (EPA, 2004, 2005), apply a different VSL 

estimate ($5.5 million in 1999 dollars, with a 95 percent confidence interval between $1 million 

and $10 million). This revised value is based on more recent meta-analytical literature, and has 

not been endorsed by the Environmental Economics Advisory Committee (EEAC) of U.S. EPA’s 

Science Advisory Board (SAB). Until U.S. EPA’s SAB endorses a revised estimate, ARB staff

continues to use the last VSL estimate endorsed by the SAB, i.e., $4.8 million in 1990 dollars. 

2

 U.S. EPA’s real income growth adjustment factor for premature death incorporates an elasticity 

estimate of 0.4.
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The U.S. EPA also uses the willingness-to-pay (WTP) methodology for some 

non-fatal health endpoints, including lower respiratory symptoms, acute

bronchitis and minor restricted activity days. WTP values for these minor

illnesses are also adjusted for anticipated income growth through 2025, although 

at a lower rate (about 0.2% per year in lieu of 0.6% per year).

For work-loss days, the U.S. EPA uses an estimate of an individual’s lost wages, 

(EPA, 2004), which ARB adjusts for projected real income growth, at a rate of 

approximately 1.5% per year.

“The Economic Value of Respiratory and Cardiovascular Hospitalizations,” 

(ARB, 2003), calculated the cost of both respiratory and cardiovascular hospital 

admissions in California as the cost of illness (COI) plus associated costs such 

as loss of time for work, recreation and household production. When adjusting 

these COI values for inflation, ARB uses the Consumer Price Index (CPI) for 

medical care rather than the CPI for all items.

Table 2 lists the valuation of avoiding various health effects, compiled from ARB 

and U.S. EPA publications, updated to 2006 dollars. The valuations based on 

WTP, as well as those based on wages, are adjusted for anticipated growth in 

real income.

Table 3: Undiscounted Unit Values for Health Effects

 (at various income levels in 2006 dollars) 1

Health Endpoint 2006 2015 2025 References

Mortality

Premature death

($ million) 8.2 8.6 9.2 (EPA, 1999), p. 70-72, (EPA, 2000), (EPA, 2004) p. 9-121)

Hospital Admissions

Cardiovascular

($ thousands) 43 48 54 (ARB, 2003), p. 63

Respiratory

($ thousands) 35 39 44 (ARB, 2003), p. 63

Minor Illnesses

Acute Bronchitis 451 459 469 (EPA, 2004), 9-158

Lower Respiratory 

Symptoms 20 20 21 (EPA, 2004), 9-158

Work loss day 189 217 252 2002 California wage data, 

U.S. Department of Labor

Minor restricted activity 

day (MRAD) 64 65 66 (EPA, 2004), 9-159

1

The value for premature death is adjusted for projected real income growth, net of 0.4 elasticity. 

Wage-based values (Work Loss Days) are adjusted for projected real income growth, as are 

WTP-derived values (Lower Respiratory Symptoms, Acute Bronchitis, and MRADs). Health 

endpoint values based on cost-of-illness (Cardiovascular and Respiratory Hospitalizations) are 

adjusted for the amount by which projected CPI for Medical Care (hospitalization) exceeds allitem CPI.
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Benefits from the proposed Commercial Harbor Craft Rule are substantial. ARB 

staff estimates the benefits to be nearly $2.0 billion using a 3% discount rate or 

$1.3 billion using a 7% discount rate. (ARB follows U.S. EPA practice in

reporting results using both 3% and 7% discount rates.) Nearly all of the 

monetized benefits result from avoiding premature death. The estimated benefits 

from avoided morbidity are less than $30 million with a 3% discount rate and less 

than $20 million with a 7% discount rate. Approximately three-fifths of the 

benefits are associated with reduced PM from direct sources, and the remaining 

two-fifths with reduced NOx. 

III. Conclusion

The health benefits of implementing the proposed regulation are substantial. 

Staff estimates that the cumulative emissions reductions over the lifetime of the 

rule can be associated with approximately 310 fewer premature deaths, 70 fewer 

hospital admissions due to respiratory causes, 120 fewer hospital admissions 

due to cardiovascular causes, 8,100 fewer cases of asthma-related and other 

lower respiratory symptoms, 670 fewer cases of acute bronchitis, 53,000 fewer 

work loss days, and 300,000 fewer minor restricted activity days. The uncertainty 

range behind each estimated benefit is on order of +/- 50%. The estimated 

statewide benefits over 2009 to 2025 from these reductions in adverse health 

effects is about $1.3 billion using a 7% discount rate or $2.0 billion using a 3%

discount rate. 
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(ARB, 1998) Air Resources Board. Proposed Identification of Diesel Exhaust as 

a Toxic Air Contaminant. Appendix III, Part A, Exposure Assessment. April 1998.

(ARB, 2000) Air Resources Board. Risk Reduction Plan to Reduce Particulate 

Matter Emissions from Diesel-Fueled Engines and Vehicles.

http://www.arb.ca.gov/diesel/documents/rrpapp.htm; October 2000.

(ARB, 2002) Air Resources Board and Office of Environmental Health Hazard 

Assessment. Public Hearing to Consider Amendments to the Ambient Air Quality 

Standards for Particulate Matter and Sulfates, Staff Report.

http://www.arb.ca.gov/research/aaqs/std-rs/pm-final/pm-final.htm; May 2002.

(ARB, 2003) Air Resources Board. Final Research Report: The Economic Value 

of Respiratory and Cardiovascular Hospitalizations. May 2003

ftp://ftp.arb.ca.gov/carbis/research/apr/past/99-329.pdf

(ARB, 2006) California Air Resources Board. Emission Reduction Plan for Ports 

and Goods Movement in California; April 2004.

http://www.arb.ca.gov/planning/gmerp/march21plan/appendix_a.pdf

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(EPA, 1999) United States Environmental Protection Agency. The Benefits and 

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Engines. EPA420-R-03-008. CD-ROM. Research Triangle Park, North Carolina. 

http://www.epa.gov/otaq/cleaner-nonroad/r03008.pdf; April 2003.

(EPA, 2004) United States Environmental Protection Agency. May, 2004. Final 

Regulatory Impact Analysis: Control of Emissions from Nonroad Diesel Engines. 

EPA-420-R-04-007. Office of Transportation and Air Quality.

http://www.epa.gov/otaq/regs/nonroad/equip-hd/2004fr.htm#ria