Calverton Office Park 11720 Beltsville Drive, Suite 900 Calverton, MD 20705-3111

Incidence and Cost 

of 

Carbon Monoxide Poisoning for All Ages, 

Pool and Spa Submersions for Ages 0−14, 

and 

Lead Poisoning for Ages 0−4 

Final Report 

Task Order 1, CPSC Contract D-09-0003 

Ted Miller, Soma Bhattacharya 

March 28, 2013

This report is being posted on the CPSC website for public comment. The 

recommendations are those of the contractor and may not reflect the views of CPSC staff. 

This report has not been reviewed or approved by, and may not necessarily reflect the 

views of, the Commission.
i 

Table of Contents

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

Data Sets and Diagnosis/Cause Codes Used .............................................................................. 1

Incidence ......................................................................................................................................... 4

Lead Poisoning............................................................................................................................ 4

CO Poisoning .............................................................................................................................. 6

Submersion ............................................................................................................................... 11

Work Loss Costs ........................................................................................................................... 17

Lead Poisoning.......................................................................................................................... 17

CO Poisoning ............................................................................................................................ 19

Submersion ............................................................................................................................... 20

Quality of Life Loss ...................................................................................................................... 23

Lead Poisoning.......................................................................................................................... 26

CO Poisoning ............................................................................................................................ 27

Submersion ............................................................................................................................... 29

Future Research ........................................................................................................................ 29

Summary ....................................................................................................................................... 30

References ..................................................................................................................................... 31

Appendix A: Other Costs of Lead Poisoning ............................................................................... 36

Appendix B: Narrative Descriptors for International Classification of Disease Codes and NEISS 

Codes Included.............................................................................................................................. 42

Codes from the 10th Edition of ICD, http://apps.who.int/classifications/icd10/browse/2010/en 

(regardless of medical treatment, multiple cause of death data typically include both a 

diagnosis code and an external cause code) .............................................................................. 42

Diagnosis Codes........................................................................................................................ 42
ii

Tables

Table 1. Incidence of Lead Poisoning at Ages 0-4 by Survival and Data Source .......................... 4

Table 2. Medically Attended Nonfatal Lead Poisonings by Case Disposition and Data Source ... 5

Table 3. Incidence of Carbon Monoxide Poisoning by Survival and Data Source ........................ 6

Table 4. Medically Attended Nonfatal Carbon Monoxide Poisoning by Case Disposition and 

Data Source ..................................................................................................................................... 8

Table 5. Incidence of Carbon Monoxide Poisoning Treated with Hyperbaric Oxygen (HBO2), 

1992−2002 ...................................................................................................................................... 9

Table 6. Incidence of Submersion by Survival and Data Source ................................................. 11

Table 7. Medically Attended Nonfatal Submersions by Case Disposition and Data Source ....... 12

Table 8. Mean Hospital Costs per Admission for Carbon Monoxide Poisoning, All Ages; Lead 

Poisoning, Ages 0−4, and Submersions, Ages 0−14, HCUP-NIS, 2007 ...................................... 15

Table 9. Mean Hospital Costs per Carbon Monoxide Poisoning Admission by Disposition, 

HCUP-NIS, 2007 .......................................................................................................................... 15

Table 10. Mean Hospital Costs per Lead Poisoning Admission by Disposition, HCUP-NIS, 2007

....................................................................................................................................................... 15

Table 11. Mean Hospital Costs per Submersion Admission by Disposition, HCUP-NIS, 2007.. 16

Table 12. IQ Points and Resulting Percentage of Earnings Lost by Blood Lead Level ............... 18

Table 13. Adverse Health Effects and Estimated Veteran’s Administration Disability Costs of 

Adult Lead Exposure by Blood Lead Level, in 2007 Dollars ....................................................... 19

Table 14. Short-Term Wage Loss and Percentage of Lifetime Earnings Lost to Traumatic Brain 

Injury by Abbreviated Injury Scale (AIS) Threat to Life Severity ............................................... 21

Table 15. Short-Term Household Production Loss and Percentage of Lifetime Household 

Production Lost to Traumatic Brain Injury by Abbreviated Injury Scale (AIS) Threat to Life 

Severity ......................................................................................................................................... 22

Table 16. Health Utility Index 2 Estimates of Utility Loss for Brain Injury by Functional Impact

....................................................................................................................................................... 24

Table 17. Utility Loss Associated with Retardation ..................................................................... 25

Table 18. Acute Symptoms in 1144 Patients with Carbon Monoxide Poisoning ......................... 27
iii

Table 19. Probability of Neurocognitive Sequelae of Carbon Monoxide Poisoning by Treatment 

Mode and Time Post-Exposure ..................................................................................................... 28

Table 20. Costs per Police-Reported Crime by Cost Category in 2010 Dollars........................... 39

Table 21. Percentage of Crimes Reported, Percentage of Reported Crimes that Lead to an Arrest, 

and Number of Arrests in 2010 ..................................................................................................... 40

Table 22. Annual Arrest Rate and Estimated Crimes Committed per Person by Age Range, 2010, 

and Estimated Annual Violent and Property Crime Costs Over Different Age Ranges per 5 μg/dl 

Rise in Blood Lead Level at Age 0−4 (in 2010 dollars) ............................................................... 41
1

Introduction

The U.S. Consumer Product Safety Commission’s (CPSC’s) major tool for estimating the 

benefits from prevention of injuries related to consumer products is its Injury Cost Model (ICM). 

CPSC developed the ICM in the late 1970s and continues to refine it. The ICM provides a 

common basis for measuring the dollar burden of a wide range of product-related injuries. Used 

in conjunction with injury and fatality data, the ICM permits the CPSC to compare alternative 

policies designed to reduce consumer product injuries and evaluate the relationships of their 

costs and benefits.

The CPSC periodically investigates issues related to swimming pool and spa submersion, 

lead poisoning, and carbon monoxide (CO) poisoning because of their frequency and severity. 

These injuries are primarily brain injuries with rare, but potentially serious long-term 

neurological sequelae. Lead poisoning also adversely affects other body systems. Unlike 

traumatic brain injuries (TBIs) (e.g., from bicycle crashes or sports), the ICM is not designed to 

capture these injuries. Thus, data on incidence and costs of health problems resulting from these 

injuries are less complete and less reliable than for most injuries associated with consumer 

products. The purpose of this task order was to improve knowledge of their incidence and costs. 

Improved estimates will enhance decision making about relevant exposures.

CPSC’s task order request focused on unintentional nonoccupational and nonfire carbon 

monoxide poisonings of victims at all ages, swimming pool and spa submersions of victims 

younger than 15 years of age, and lead poisonings of victims younger than 5 years of age. The 

task order called for analyses of incidence of medically treated cases, associated work losses, and 

quality-of-life losses, and acute, but (due to budget constraints) not long-term, medical care costs

for cases associated with products under CPSC’s jurisdiction. Lead poisoning has other sequelae,

including increased need for special education and elevated risk of occurrence of attention deficit

hyperactivity disorder (ADHD) and criminal behavior. The appendix examines the rates and 

costs of those events.

Data Sets and Diagnosis/Cause Codes Used 

We primarily used Healthcare Cost and Utilization Project (HCUP) and National 

Electronic Injury Surveillance System (NEISS) data. HCUP is a family of health care databases 
2

and related software tools and products developed through a federal-state-industry partnership 

and sponsored by the Agency for Healthcare Research and Quality (AHRQ). We analyzed 2006 

HCUP-KID (kid’s inpatient database), 2007 HCUP NIS (nationwide inpatient sample), and 2007 

HCUP NEDS (nationwide emergency department (ED) sample).1 NEISS is the CPSC’s EDbased injury surveillance system. It draws data from a much smaller sample of EDs than NEDS, 

but it investigates cases in far greater detail. Unlike the HCUP data sets, NEISS contains 

narratives that can be used to differentiate swimming pool and spa submersions from other 

submersions. For submersions, therefore, we also used 2008 NEISS consumer product injury and 

all-injury profile (AIP) data.

We obtained and incorporated data from the Undersea and Hyperbaric Medical Society 

(UHMS) hyperbaric oxygen treatment database (a joint project with the Centers for Disease 

Control and Prevention (CDC)) for treatment of CO poisoning cases. We also examined CO 

poisoning incidence reported in the National Poisoning Data System (NPDS) operated by the 

American Association of Poison Control Centers.

In the United States, mortality data are coded by diagnoses, intent, and cause/mechanism 

of injury/poisoning using International Classification of Diseases, 10th Edition (ICD10). 

Hospital inpatient and emergency department discharge data are coded with this information 

using the older International Classification of Diseases, 9th Edition, Clinical Modification 

(ICD9-CM). Coding of hospital data will move to ICD10-CM on October 1, 2014. Appendix B 

lists ICD codes used in this project.

We drew fatal and ED-treated submersion incidence and location data from published 

sources: the CPSC’s analysis of 2006−2008 National Vital Statistics System (NVSS) mortality 

data; 2008−2010 NEISS consumer product injury data and supplemental NEISS investigations 

(Gipson 2011a, 2011b); and the CDC’s analysis of 2005−2009 NVSS and NEISS-AIP data

(Laosee et al. 2012). All three studies searched text narratives to determine place of submersion.

Unintentional, non-transport, nonfatal submersion injuries in NEISS and NEISS-AIP cases were 

defined as cases with NEISS injury code 64. CPSC and CDC identified fatal submersions as 

 

1

 Adjustments were required for the state of Texas, which provided age categories rather than actual ages. For lead 

poisoning at ages 0−4, we used the Texas count of lead poisoning patients in age categories 1 and 2 (ages 0−17) 

times percentage of patients ages 0−4 among those ages 0−17 in all other states. We used a parallel computation for 

submersions. 
3

ICD10 codes W16, W29, W65, W66, W73, W74, or Y21 and also searched narrative fields for 

the terms “drown” or “submer.” CPSC and CDC used NEISS product codes and NEISS and 

NVSS narratives to identify pool and spa submersions. (See Appendix B for ICD and NEISS 

codes descriptors.)

We tabulated lead poisoning fatalities (ICD10 code T56.0) with 2009 NVSS data. For 

CO poisoning, we used a CPSC CO fatality count restricted to nonfire deaths associated with the 

use of consumer products under CPSC’s jurisdiction (Hnatov 2012). This count started from all 

cases with diagnosis code X47 or Y17. CPSC searched accompanying death certificate narratives 

to identify CO cases and determine their etiology. We also give a broader CO fatality count for 

ICD10 diagnosis code T58, modified by external cause codes X47 or Y17, and excluding 

uncontrolled fire deaths and deaths in motor vehicles. This count includes all remaining 

unintentional CO deaths and an allocated portion of deaths of undetermined intent.

In analyzing hospital and ED discharges using HCUP, we excluded cases paid by 

Worker’s Compensation. Among nonoccupational cases, unintentional, non-transport, nonfire 

CO poisoning cases were defined as cases with an ICD9-CM external cause code between 

E868.2 and E868.9 or with diagnosis code 986, as well as an external cause code of E868.1 or 

E868.2. Lead poisoning was defined to be cases with diagnosis 984 and/or external cause code 

E861.5 or E866.0. Submersion was defined as cases with diagnosis 994.1 and/or external cause 

code E830, E832, or E910. ICD9-CM does not distinguish swimming pool and spa submersions 

from bathroom, bucket, and open body of water submersions.

Lead exposure is most often chronic, not acute, without obvious symptoms. Indeed, most 

lead exposure cases are not medically attended or even recognized as occurring. Therefore, we 

also drew on national surveillance data on lead poisoning to estimate low-level exposure. 
4

Incidence

As prescribed in CPSC’s task order, this chapter largely focuses on counts of the 

medically treated injuries used to gain insight into medical treatment cost and outcome issues. 

Those interested in the subset of incidents associated with consumer products under CPSC 

regulation should consult the CPSC reports cited below. Among medically treated nonfatal cases, 

submersion incidence was highest, followed by CO poisoning, and then lead poisoning. 

Lead Poisoning 

Childhood lead poisoning is rarely fatal, with no fatalities under age nine in 2007−2010. 

Tables 1 and 2 present incidence of lead poisoning in children ages 0−4 both for hospital-treated 

fatal and nonfatal cases, as well as for nonfatal cases, by location of disposition. These events are 

rare. We recommend relying on the KID dataset for hospital-admitted lead poisoning (and child 

submersion) incidence counts because its sample size of child cases is much larger than in the 

2007 HCUP–NIS, resulting in narrower confidence intervals. The NEDS estimate of lead 

poisoning admissions 

Table 1. Incidence of Lead Poisoning at Ages 0-4 by Survival and Data Source 

Data 

source Year

Fatal or 

Nonfatal

Raw 

Case 

Count

Weighted 

Incidence

Linearized 

Standard 

Error

[95% 

Confidence 

Interval]

NVSS 2007-

2010 Fatal 0 0 0 0 0

NIS 

Inpatient 

Sample

2007 Nonfatal 51 247 69 111 384

Fatal 0 0

NEDS ED 

Visit 

Sample

2007

Treated & 

Released 10 45 *

Admitted 17 84 *

Fatal 0 0

KID Child 

Inpatient 

Sample

2006 Nonfatal 120 211 34 144 279

Fatal 0 0

NB: NIS (nationwide inpatient sample) and KID (kid’s inpatient database) fatality counts are restricted to patients 

admitted to the hospital. NEDS counts only those fatalities where the victims died in the ED. KID counts only 

patients under age 21.* Empty strata prevented variance estimation.
5

is less reliable; it is based on such a small count that we could not estimate its standard error. The 

very low count of lead poisoning cases in EDs is matched by a virtual absence of cases in 

doctors’ offices in National Ambulatory Medical Care Survey (NAMCS) data. NAMCS is an

annual U.S. National Center for Health Statistics survey.

During 1999–2004, 1.4 percent of children ages 1–5 years had blood lead levels at least 

10 micrograms per deciliter (μg/dL) (Jones et al., 2009). National data, collected in 2007–2008 

(CDC, 2012), show that the median blood lead level (BLL) in children ages 1–5 years is 1.4 

μg/dL; the 95th percentile is 4.1 μg/dL. Although children with BLLs in this lower range are 

unlikely to be medically attended, as documented in the wage loss section below, low lead 

exposure reduces IQ.

Table 2. Medically Attended Nonfatal Lead Poisonings by Case Disposition and Data Source 

Data 

source Year

Agegroup Disposition

Raw 

Case 

Count

Weighted 

Incidence

Linearized 

Standard 

Error

[95% 

Confidence 

Interval]

Hospital-admitted

NIS 2007 0−4 Discharged to Home 45 220

NIS 0−4 Discharged to 

Nursing Home*

0 0

NIS 0−4 Discharged to 

Another Facility**

0 0

NIS 0−4 Discharged to Home 

Health Care

6 28

Hospital-admitted

KID 2006 0−4 Discharged to Home 111 195 30 136 254

KID 0−4 Discharged to 

Nursing Home*

0 0 0 . .

KID 0−4 Discharged to Home 

Health Care

9 16 13 0 42

Note: Missing standard error due to stratum with single nonzero sampling unit.

* Nursing home includes both skilled nursing facilities and intermediate care facilities.

**The definition of another facility varies by state and may include residential care, hospice 

facility, rehabilitation center, psychiatric hospital, or other non-acute care.
6

CO Poisoning 

Table 3 presents incidence data about CO poisoning. For 2007 to 2009, based on a handreview of death certificates, CPSC estimates unintentional nonfire CO poisoning deaths 

associated with consumer products under CPSC’s jurisdiction averaged 169 per year (Hnatov 

2012). NVSS indicates that an average of 477 people per year died of unintentional CO 

poisoning in 2007 to 2008 (excluding deaths in uncontrolled fires and motor vehicles). This 

estimate includes 14 deaths per year allocated from the undetermined intent category and 3.5 

deaths per year involving carbon monoxide poisoning (ICD10 code T58) without codes that 

would indicate they were intentional or related to fires or motorized vehicles. That suggests 

roughly 35 percent of unintentional CO poisoning deaths not associated with fires or motor 

vehicles involve consumer products regulated by CPSC. That same percentage might apply to 

nonfatal cases. (Including intentional exposures and fire-related cases, CO deaths in 2007 to 

2008 totaled 3,745.)

Table 3. Incidence of Carbon Monoxide Poisoning by Survival and Data Source 

Data source Year

Fatal or 

Nonfatal

Agegroup

Raw 

Case 

Count 

Weighted 

Annual 

Incidence

Linearized 

Standard 

Error

[95% 

Confidence 

Interval]

NVSS + Death 

Certificates 

(Hnatov 2012)

2007-

2009

Fatal

Consumer 

Product

All 508 169 12 118 221

NVSS

2007-

2008 Fatal All 954 477 NA NA NA

HCUP NIS 2007 Nonfatal All 243 1,210 186 846 1,574

Inpatient

Sample Fatal All 6 30 12 6 53

HCUP NEDS

ED 2007

Treated & 

Released All 2,752 13,029 742 11,574 14,485

Visit Sample Admitted

Fatal

All

All

283

4

1,296

21

112

11

1,075

0

1,517

43

HCUP KID 

Child 2006 Nonfatal 0−20 93 153 25 105 201

Inpatient

Sample Fatal 0−20 2 3 2 0 8

NB: NA=Not Applicable (vital statistics counts are a census; HCUP = Healthcare Cost and Utilization Project, NIS 

=nationwide inpatient sample, NEDS = nationwide emergency department sample, KID = kid’s inpatient database. 

NIS and KID fatality counts are restricted to patients admitted to the hospital. NEDS fatalities died in the ED; NEDS 

does not track patients beyond hospital admission.
7

HCUP-NIS estimates 1,210 people were discharged alive after hospital inpatient stays for 

unintentional nonfire CO poisoning in 2007. According to HCUP KID, 153 of those survivors 

were children. NIS and KID show that almost none of the deaths occurred in hospital inpatient 

units. Finally HCUP-NEDS─which is an independent sample, not a subset of NIS─estimates that 

more than 14,000 CO poisoning patients were treated in the ED; an estimated 1,296 of these 

patients were admitted to a hospital and 21 died in the ED. The remainder were treated and 

released. NIS estimates about 30 died in the hospital after being admitted. It is not surprising that 

NIS and NEDS yield consistent estimates. Neither is a national probability sample. The NEDS 

emergency department sample (including cases admitted through the ED and cases that instead 

were treated and released) comes from a subset of the states that have NIS inpatient data, 

although the two systems sample cases from different data sets. In states included in both data 

sets, NEDS samples a much larger share of admissions through the ED, but it misses any 

admissions that bypass the ED (e.g., if a hospital admitted the patient directly to a hyperbaric 

chamber). HCUP weights both samples using the same procedures.

Table 4 shows discharge destinations for hospital-admitted CO poisoning survivors. 

Patients discharged to places other than home typically have lasting disability. Effects of CO 

poisoning, however, are not always clear-cut during initial treatment. After initially appearing to 

have made a full recovery based on restoration of normal carboxyhemoglobin levels, even 

treated and released ED patients can experience delayed neurological sequelae resulting in 

lasting impairment. This is also true for patients treated with hyperbaric oxygen (HBO2). 

Symptoms may not manifest until well after the patient returns home.

CO poisoning treatment generally involves administering oxygen, either normobaric 

(face mask at ambient pressure) or hyperbaric (high-pressure chamber). HCUP CO incidence 

(and related medical cost) estimates may miss some cases that receive hyperbaric oxygen 

treatment. Table 5 presents incidence of CO poisoning treated in hyperbaric treatment facilities 

between 1992 and 2002 (Hampson and Little, 2005). On average, approximately1,500 cases, 

including fire-related and intentional CO poisonings, annually received one hyperbaric treatment, 

with a few receiving a second treatment. Of 1,907 survivors treated in a large convenience 

sample of 64 hyperbaric facilities between August 2008 and July 2011, 45 percent were treated 

and released (Hampson et al., 2012). Those patients probably would be missed in studies relying 

on hospital and ED discharge data. Wide variations in hyperbaric facility usage rates between 
8

states (Hampson et al., 2012) suggest usage probably is determined by physician preference and 

facility presence more than by patient health status.

In 2008, the Centers for Disease Control and Prevention (CDC) teamed with the 

Undersea and Hyperbaric Medical Society (UHMS) to monitor cases of carbon monoxide 

poisoning treated in U.S. hyperbaric facilities (Hampson et al., 2012). This system went live 

nationally and was open voluntarily to all U.S. hyperbaric facilities on August 1, 2008. Given the 

estimates from Table 5, it probably captures around 42 percent of cases annually (636/1500). 

Exhibit 1 presents surveillance system data from Hampson et al. (2012), showing incidence, 

patient demographics, and details of exposure and treatment. These data probably were 

representative of hyperbaric use in their catchment areas. Importantly, 68 percent of cases were 

unintentional nonfire, non-motor-vehicle (auto or boat) cases. Most nonoccupational cases in this 

category resulted from defective furnaces and improper use of generators. Intubation often 

means the patient was unconscious when hyperbaric treatment began, but it may not necessarily

imply a bad outcome.

Table 4. Medically Attended Nonfatal Carbon Monoxide Poisoning by Case Disposition and Data 

Source 

Data 

source Year

Agegroup Disposition

Raw 

Case 

Count

Weighted 

Incidence

Linearized 

Standard 

Error

[95% 

Confidence 

Interval]

Hospital-admitted only

NIS 2007 All Discharged to Home 208 1029 158 719 1339

NIS All Discharged to 

Nursing Home

0 0 . . .

NIS All Discharged to 

Another Facility*

22 113 31 51 174

NIS All Discharged to Home 

Health Care

13 68 19 32 105

Hospital-admitted

children only

KID 2006 0−20 Discharged to Home 89 147 24 99 195

KID 0−20 Discharged to 

Nursing Home

3 4 3 0 11

KID 0−20 Discharged to Home 

Health Care

1 2 2 0 4

Note: Missing standard error due to stratum with single nonzero sampling unit
9

*The definition of another facility varies by state and may include residential care, hospice 

facility, rehabilitation center, psychiatric hospital, or other non-acute care.

Table 5. Incidence of Carbon Monoxide Poisoning Treated with Hyperbaric Oxygen (HBO2), 

1992−2002 

Year Patients with CO Poisoning

Annually Treated with HBO2

1992 1291

1993 1450

1994 1502

1995 1714

1996 1684

1997 1448

1998 1492

1999 1452

2000 1441

2001 1388

2002 1505

Source: Hampson and Little (2005). 
10

Exhibit 1. Demographic Characteristics of Carbon Monoxide Poisoning Patients in the 

(Voluntary) National Hyperbaric Oxygen Surveillance System, 8/1/2008−7/31/2011 

 One thousand nine hundred seven cases were reported between August 1, 2008 and July 31, 

2011.

 The six states that reported the most cases are: Utah (197), Pennsylvania (189), Washington 

(169), Michigan (146), Illinois (144), and Maryland (139).

 The incidence by gender is 1,128 males (59%), 787 females (41%), including 46 pregnant 

women (total of 1915 conflicts with other counts in Hampson et al, 2012). 

 A total of 59.6 percent of cases were non-Hispanic whites.

 Among 1,513 cases responding to this question, 3.7 percent had experienced prior CO 

poisoning. 

 Furnace (38%), generator (20%), and fire (13%) were the three most common sources of 

nonoccupational, non-transport-related CO poisoning cases. Together they accounted for 71 

percent of those cases. 

 Of known cases, 1,505 (85%) were unintentional (including fire and motor vehicle), and 273 

(15%) were intentional. 

 Occupational incidents (292) accounted for 15 percent of cases. 

 Virtually all cases already had been treated with normobaric oxygen. 

 A total of 15.7 percent of cases were intubated. 

Age Distribution (1,905 cases with known ages) 

Age Group Cases Percent

0−9 167 8.8%

10−19 203 10.7%

20−29 279 14.6%

30−39 295 15.5%

40−49 362 19.0%

50−59 275 14.4%

60−69 170 8.9%

70−79 92 4.8%

80−89 57 3.0%

90+ 5 0.3%

Source: Hampson et al. (2012). 
11

Submersion 

Table 6 presents submersion incidence in children ages 0−14, for fatal and non-fatal

discharges from the ED, and Table 7 breaks these cases down by place of disposition. In Table 

7, ED data systems record whether children were admitted to the hospital but do not track status 

post-admission. NIS and KID show discharge destinations and survival for these cases. NEDS’s

estimate of child submersion cases treated and released, which comes from a much larger sample 

(1617 cases versus 101 for NEISS, Consumer Product Sample (CPS) and 32 for NEISS-AIP) and 

far more EDs than the NEISS estimates, is two to three times the NEISS CPS and NEISS AIP 

estimates and exceeds their 95 percent confidence intervals. In contrast, admission estimates 

(weighted incidence) from the five data systems range from 1,951 to 2,586, with the preferred 

KID estimate at 2,107, including 1,914 non-fatal discharges and 203 deaths in the hospital.

Table 6. Incidence of Submersion by Survival and Data Source 

Data 

source Year

Fatal or 

Nonfatal

Agegroup

Raw 

Case 

Count

Weighted

Incidence

Linearized

Standard 

Error

[95% Confidence 

Interval]

NIS 2007

Nonfatal

Inpatient 0−14 375 1805 297 1223 2387

Inpatient 

Sample 2007 Fatal 0−14 38 178 . . .

NEISSCPS ED 

Consumer 

Product 

Sample 2008

Nonfatal

ED 0−14 185 4981 1616 1771 8192

NEISS-AIP

ED All 

Injury 

Sample 2008

Unintentional 

Nonfatal

ED 0−14 103 3536 817 1936 5136

NEDS 2007

Nonfatal

ED 0−14 2180 10083 . . .

ED Sample 2007 Fatal 0−14 98 452 . . .

KID Child 2006

Nonfatal

Inpatient 0−14 1160 1914 135 1650 2179

Inpatient 

Sample 2006 Fatal 0−14 121 203 26 153 253
12

Table 7. Medically Attended Nonfatal Submersions by Case Disposition and Data Source 

Data 

source Year

Agegroup Disposition

Raw 

Case 

Count

Weighted 

Incidence

Linearized

Standard 

Error

[95% 

Confidence 

Interval]

NIS 2007 0−14 Admission Discharged 

to Home

365 1755 289 1189 2322

NIS 2007 0−14 Discharged to Nursing 

Home or Another 

Facility*

0 0 . . .

NIS 2007 0−14 Discharged to Another 

Institution

3 14 . . .

NIS 2007 0−14 Discharged to Home 

Health Care

7 35 . . .

NEISSCPS2008 0−14 ED Treated & 

Released-All

101 2783 895 1005 4561

NEISSCPS2008 0−14 ED Treated & 

Released-Injured at 

Home

53 1521 521 486 2555

NEISSCPS2008 0−14 Admitted thru ED-All 84 2198 795 619 3777

NEISSCPS2008 0−14 Admitted thru EDInjured at Home49 1490 653 192 2788

NEISSAIP2005 0−14 ED Treated & 

Released-All

32 1169 354 460 1878

NEISSAIP2005 0−14 ED Treated & 

Released-Injured at 

Home

5 88 41 5 171

NEISSAIP2005 0−14 Admitted thru ED-All 49 1951 551 848 3054

NEISSAIP2005 0−14 Admitted thru EDInjured at Home24 877 269 339 1415

NEDS 2007 0−14 ED Treated & Released 1617 7496 . . .

NEDS 2007 0−14 Admitted thru ED 563 2586 . . .

KID 2006 0−14 Admission Discharged 

to Home

1112 1835 130 1580 2091

KID 2006 0−14 Discharged to Nursing 

Home or Another 

Facility*

30 49 10 29 69

KID 2006 0−14 Discharged to Home 

Health Care

18 30 7 16 43

Note: Missing standard error due to stratum with single nonzero sampling unit 

* The definition of another facility varies by state and may include residential care, hospice 

facility, rehabilitation center, psychiatric hospital, or other non-acute care. 
13

Admitted submersion cases with sequelae almost always emerge dependent on 

tracheotomy tubes and possibly feeding tubes. This means these children have expected short 

lifespans, cannot breathe independently, typically require round-the-clock nursing care, and are 

medically fragile and prone to infection. 

Based on narrative record review, Laosee et al. (2012) estimate that at ages 0−4, 50.1 

percent of deaths and 64.6 percent of ED visits for submersion result from pool and spa 

incidents. Among nonfatal events, they estimate 45.7 percent are in private pools; 31.7 percent 

are in public pools; and 22.6 percent are in unspecified pools. At ages 5−14, they estimate 29.9 

percent of deaths and 76.0 percent of ED visits are pool-related submersions. The pattern among 

pool types differs with only 20.8 percent in private pools; 62.4 percent in public pools; and 16.8

percent in pools of unspecified type. Overall, at ages 0−14, 43.4 percent of drowning deaths and

67.8 percent of nonfatal submersions occur in pools and spas. Gipson (2011a) estimates pool and 

spa fatalities under age 15 averaged 383 in 2006−2008, higher than the Laosee et al. estimate of 

332 per year (with place of occurrence unknown for many cases). (Another 351 pool submersion 

deaths occurred annually among adults.) Gipson (2011b) further estimates 660 non-pool and 

non-spa submersion incidents occurred in 2005–2009 for children younger than 5 years old. 

These include 431 fatalities, 212 nonfatal injuries, and 17 incidents with no apparent injury or 

unknown injury.

Short-Term Medical Costs 

Tables 8−11 present the mean costs of acute medical care for hospital admissions for the 

target conditions. We computed costs by multiplying hospital-and-service-specific cost-to-charge 

ratios developed by AHRQ times charge data on NIS. We generally did not add separately 

charged professional fees and post-discharge costs. CPSC’s Injury Cost Model (ICM) estimates 

lifetime medical costs of a hospital-admitted nonfatal injury by multiplying acute inpatient costs 

times the ratio of total costs, including inpatient costs, professional fees, and post-discharge 

costs, to acute costs. The last column in Table 8 shows the ratios the ICM uses for CO 

poisoning, lead poisoning, and submersion. the ratios of total costs – including inpatient costs, 
14

professional fees, and post-discharge costs – to inpatient costs that our existing injury cost 

algorithm would multiply, times hospital inpatient costs, to estimate lifetime costs. Reliability of 

those ratios is uncertain for the conditions under study. It was originally planned to analyze

diagnosis-specific utilization/medical payments in a claims file to provide better estimates, but 

lack of funding precluded this analysis.

Among admitted cases, acute medical costs per case were highest for submersion, 

followed by CO poisoning, with lead poisoning much lower (Table 8). For nonfatal submersion, 

we could not establish case severity because HCUP datasets lack the five-digit procedure codes 

needed to identify cases requiring critical care or ventilator management. Data sparseness also 

prevented us from calculating standard errors. 

In 1998, average Medicare payments for a covered hyperbaric treatment of CO poisoning 

were approximately $405, including $140 for physician supervision and $265 for outpatient 

services (Office of Inspector General, 2000). Hampson and Little (2005) estimate most patients 

receive only one treatment. 

Quest Laboratories charges the military and other volume purchasers $6−$7 for a blood 

lead test, with retesting indicated if blood lead level (BLL) exceeds 35−40 μg/dL. Although 

CDC only recommends chelation therapy if child BLL exceeds 45 μg/dL, concerns about effects 

of lower BLLs has increased use on lesser exposures, despite potential side effects. A single 

chelation treatment usually lasts 2−4 hours. It cost $77 on average in 2007 (Nahin et al. 2009). In 

the first month, patients typically receive 5−30 treatments, with 30 being most common (Keogh 

& Boyer 2011). Thus, the typical cost is around $2,000. 

By design, this task order did not probe the costs of care in the post-acute period. 

Estimating those costs would require a longitudinal analysis of a very large claims file like a 

multistate Medicaid file. That analysis also would greatly improve our knowledge of the severity 

distribution and of survival time following catastrophic injury. 

A parent gave us permission to disclose long-term medical costs of her child’s 

submersion injury that occurred in California in July 1979 when he was 14 months old. He is 

tracheotomy-dependent and tube-fed. He spent his first year post-injury in hospital. He then 

came home to 24-hour registered nursing (RN) care at $8 per hour. The mother sued and got him 

admitted to school; the schools paid his nurse as an attendant. He was home for 25 years with 24-
15

hour nursing care. Because RNs now cost $40/hour in California, the mother has been forced to 

shift her son to a subacute hospital facility with costs of $18,000 per month. Consistent with this 

anecdote, life care planners tell us that $8 million in lifetime medical costs is typical as a 

plaintiff’s claim for cases related to catastrophic birth outcomes that involve similar care needs.

Table 8. Mean Hospital Costs per Admission for Carbon Monoxide Poisoning, All Ages; Lead 

Poisoning, Ages 0−4, and Submersions, Ages 0−14, HCUP-NIS, 2007 

Agegroup

Type of Case Mean Hospital Costs

(2007$)

Lifetime Medical Cost 

Multiplier*

All CO Poisoning 15,769 1.86

0−4 Lead Poisoning 7,857 1.73

0−14 Submersions 25,896 3.36

* This multiplier is the ratio of lifetime medical costs, including professional fees and post-discharge care 

to acute hospital care from PIRE’s existing injury cost models. 

Note: Missing standard error due to stratum with single sampling unit.

Table 9. Mean Hospital Costs per Carbon Monoxide Poisoning Admission 

by Disposition, HCUP-NIS, 2007 

Disposition Mean Hospital Costs

(2007$)

Discharged to Home 9,657

Discharged to Another Institution 70,588

Discharged to Home Health Care 17,542

Table 10. Mean Hospital Costs per Lead Poisoning Admission 

by Disposition, HCUP-NIS, 2007 

Disposition Mean Hospital Costs

(2007$)

Discharged to Home 7,131

Discharged to Home Health Care 13,654
16

Table 11. Mean Hospital Costs per Submersion Admission by

Disposition, HCUP-NIS, 2007 

Disposition Mean Hospital Costs

(2007$)

Discharged to Home 22,438

Discharged to Another Institution 130,346

Discharged to Home Health Care 156,453
17

Work Loss Costs 

This section provides the present value of future productivity losses (wage work and 

household work) at 3 percent and 7 percent discount rates. 

Lead Poisoning 

The relationship between childhood lead poisoning and subsequent IQ loss is well 

established in the literature. Attention originally focused on productivity losses associated with 

child blood lead levels (BLL) ≥ 10 μg/dl (Grosse, 2002; Gould, 2009, Needleman, 2004; Pocock 

et al., 1994; Schwartz, 1994a; Schwartz, 1994b). More recent research documents impacts of 

lower range BLLs of 2−10 μg/dl (Canfield et al., 2003; Lanphear et al., 2005).

Lanphear et al. (2005) is widely accepted as the definitive study (CPSC, 2012; EPA, 

2006; Gould, 2009; Muennig, 2009). It estimates a nonlinear relationship between increasing 

lead exposure and changes in IQ. “Estimated IQ point decrements associated with an increase in

blood lead from 2.4 to 10 μg/dL, 10 to 20 μg/dL, and 20 to 30 μg/dL were 3.9 (95% CI, 2.4–5.3), 

1.9 (95% CI, 1.2–2.6), and 1.1 (95% CI, 0.7–1.5), respectively. For a given increase in blood 

lead, the lead-associated intellectual decrement for children with a maximal blood lead level < 

7.5 μg/dL was significantly greater than . . . for those with a maximal blood lead level ≥ 7.5 

μg/dL (p = 0.015).” With adjustment for covariates, the best-fitting model resulted in a 

relationship between BLL and change in IQ given by:

Change in IQ = ln(BLL)*(-2.7).

Consistent with these findings, Chandramouli et al. (2009) established that lead poisoning 

adversely affects academic performance and echoed findings by Chen et al. (2007) that it causes 

behavioral problems. Importantly, Dietrich et al. (2004) found that chelation therapy did not 

reduce the long-term neuropsychological and behavioral effects of child lead poisoning. 

Muennig (2009), Grosse (2002), and Schwartz (1994b) (all relying heavily on classic 

work by Needleman) directly analyzed the impact of lower IQ levels on future earning potential. 

Like IQ impact, this relationship is relatively invariant over time. Thus, future work loss cost can 
18

be estimated by applying their estimates of percentage impact on average potential earnings and 

household production per IQ point lost to CPSC’s lifetime productivity estimates by age and sex. 

Muennig (2009) concludes that Schwartz (1994b) uses the soundest design for assessing 

the impact of lower IQ levels on future earning potential. Schwartz (1994b) estimated that a onepoint difference in IQ results in a 1.76 percent difference in earnings, an estimate that also 

accounts for a differential rate of high school graduation. Grosse et al. (2002) calculate that 

analyses in Salkever (1995) indicate the difference averages 2.37 percent, while Neal and 

Johnson (1996) estimate the difference averages 1.66 percent. So earnings loss for a given BLL 

change would be (ln(BLLpost)-ln(BLLpre))*(-2.7) * .0176 * lifetime earnings.

We recommend that the CPSC estimate productivity losses from its lifetime earnings 

estimates, assuming an initial BLL of one. Table 12 shows how the losses of IQ points 

associated with various blood lead levels determine earnings losses. The age-earnings model 

built into the CPSC’s ICM estimates lifetime productivity at age 2 averages $939,691, including

$653,559 in wages and $286,132 in household production (present value at a 3 percent discount 

rate, in 2007 dollars). These estimates exclude productivity loss associated with other chronic 

health effects of lead exposure.

Table 12. IQ Points and Resulting Percentage of Earnings 

Lost by Blood Lead Level 

Blood Lead Level ( ug /dL) IQ Points Lost % of Earnings Lost

2 1.9 3.3%

5 4.3 7.6%

7 5.3 9.2%

10 6.2 10.9%

20 8.1 14.2%

30 9.2 16.2%

40 10 17.5%

50 10.6 18.6%

60 11.1 19.5%

90 12.1 21.4%

Earnings Loss Unrelated to IQ Loss. Although the task order focuses on childhood lead 

poisoning, some cases will continue undiagnosed into adulthood for two reasons. First, chelation 

therapy reduces but does not eliminate blood lead. Second, some parents decline chelation. 

Moreover, although a month of intensive treatment often is indicated, side effects or other 

burdens on parents and the exposed child may lead to drop out mid-course. For analyses that 
19

need to account for enduring effects of lead exposure, Table 13 summarizes signs and symptoms 

by BLL. Of greater relevance, the table estimates net present value of disability payments that 

the Veteran’s Administration would make to a claimant by BLL. Those payments proxy lost 

earnings due to the listed health effects. 

Table 13. Adverse Health Effects and Estimated Veteran’s Administration Disability Costs of Adult 

Lead Exposure by Blood Lead Level, in 2007 Dollars 

BLL (μg/dL) Signs & Symptoms Making Onset Disability Cost/VA Claim

<10 ALAD* inhibition, linear homocysteine level rise with BLL, 

nephrotoxicity, increased risk for ischemic heart disease, 

hypertension, and end-stage renal disease; decreased glomerular 

filtration rate; adverse pregnancy outcomes including spontaneous 

abortion, decreased birth weight and head circumference

15−20 Erythrocyte protoporphyrin increases, EPO inhibition; subtle, nonspecific neurologic effects at 20-60 μg/dL$15,075

30 Increased simple reaction time, cognitive CNS deficits, anemia,†

peripheral nerve dysfunction, proteinuria, enzymuria, hypertension; 

changes in FSH, LH and testosterone levels; changes in immune 

parameters

$58,685

40 Increases in urinary ALA and coproporphyrin, sperm changes, gout, 

decreased fertility. Changes in T4 and TSH levels. Neurobehavioral 

changes

$148,237

50 Decreased hemoglobin production, disturbed sleep, anorexia $262,915

60 Abdominal pain, arthralgia, clumsiness, vomiting, irritability, 

inability to concentrate, fatigue, diarrhea, headache, behavioral 

changes, inhibition of Vitamin D activity, severe renal disease with 

chronic exposure

$374,631

80 Frank anemia $416,626

100–120 Ataxia, vomiting, convulsions, stupor, constipation, coma; mental 

retardation, epilepsy, blindness, sterility, severe renal damage

$664,017

*Abbreviations: ADD (attention deficit disorder); ALA (5-aminolevulinic acid); ALAD (δ-aminolevulinic acid 

dehydratase); EPO (erythropoietin); FSH (follicle-stimulating hormone); Ig (immunoglobulin); LH (luteinizing 

hormone);T4 (thyroxine); TSH (thyroid stimulating hormone) 

†Anemia can appear at BLLs as low as 20 μg/dL, but may be more commonly associated with higher levels (50-80 

μg/dL).

Source: Compiled from various VA disability scales and coding systems and analyzed by the author. 

CO Poisoning 

Surprisingly, although many studies (reviewed in the section on quality of life loss) have 

analyzed longer term impairments associated with CO poisoning, a literature search did not 

reveal data about impact on work-related disability. Data on 92 jury verdicts in carbon monoxide 

cases included only three, where past wage losses were stated, with losses of $3,600, $49,947, 

and $95,500. We gained additional insight by calling a leading forensic specialist in vocational 
20

rehabilitation (VR), Robert Taylor. Mr. Taylor reports that brain damage severity is strongly 

predicted by carboxyhemoglobin level at intake and that brain damage often is diffuse and quite 

severe in its impact. We suggest a reasonable assumption might be a 15 percent loss in earning 

capacity (proportional to the quality of life loss estimate below) for those with enduring 

cognitive sequelae. Hampson et al. (2009) report that regardless of severity, nonfatal CO 

poisoning does not shorten lifespan, although lifestyle factors cause those experiencing CO 

poisoning (including intentional self-harm) to have elevated risks of subsequent death from 

suicide, violence, substance abuse, or unintentional injury.

For people with the age and sex distribution of CO poisoning victims from Exhibit 1, the 

age-earnings model built into CPSC’s ICM predicts lifetime productivity would average 

$937,815. This includes $640,282 in wages and $297,533 in household production (present 

value at a 3 percent discount rate, in 2007 dollars). A 15 percent lifetime earnings loss equates to 

$140,672, including $96,042 in wages and $44,630 in household production.

Submersion 

For submersion, children with severe sequelae generally do not survive to working age, 

meaning their lifetime productivity is lost (Zamula, 1987). Unless the child is placed in 

residential care, one parent also typically will lose the majority of their productivity until the 

child dies. 

Our current injury cost model includes imperfect estimates of probability of work-related 

disability for hospital-admitted submersion survivors with moderate sequelae. The best data 

available are the broadly based but not-fully-representative submersion estimates in Zamula 

(1987). We supplemented that information with estimates by VR specialist Robert Taylor. Cases 

with severe sequelae require 24-hour skilled nursing care and greatly reduce lifespan. Mr. Taylor 

tells us that submersion cases with moderate (as opposed to severe) sequelae are rare, maybe 2

percent of those with sequelae—and those involve substantial deficits, even though the child is 

ambulatory. National Drowning Prevention Alliance Advisory Council Chair Nadina Riggsbee 

had similar impressions and reported that pediatricians generally tell parents that typical survival 

is 6 years. The longest surviving patient with severe sequelae currently is in his 34th year.
21

The sequelae of submersion are brain injuries. Therefore, one alternatively could 

calculate the cost of submersion injuries with the work loss estimates for ages 0−4 developed for 

CDC for traumatic brain injury of different severities (Miller et al., 2009). In 2000 dollars, the 

short-term earnings losses (which should approximate parental work loss) and percentage of 

lifetime earnings lost appear in Table 14. Table 15 shows equivalent information for household 

production. Unfortunately our only insight into the traumatic brain injury (TBI) severity 

distribution for submersion injuries is information from key informants Taylor and Riggsbee.

That information suggests that 98 percent of the cases might face 100 percent disability (meaning 

it is associated with 100 percent loss and is not covered in Tables 14-15; and 2 percent might be 

Abbreviated Injury Scale 3 (AIS 3, http://www.trauma.org/archive/scores/ais.html) (e.g., a case 

that resulted in deafness).

Table 14. Short-Term Wage Loss and Percentage of Lifetime Earnings Lost to 

Traumatic Brain Injury by Abbreviated Injury Scale (AIS) Threat to Life Severity 

AIS Admitted ED & Released Outpatient Dept MD Office All

Short-Term Earnings Loss (in 2000 dollars)

1-Minor Injury $2,289 $1,229 $82 $112 $842

2-Moderate Injury $2,179 $468 $86 $285 $686

3-Serious Injury $3,561 $1,926 $242 $2,600

4-Severe Injury $3,000 $550 $412 $2,016

5-Critical Injury $3,613 $3,613

Percentage of Lifetime Earnings Lost

1-Minor Injury 6.811% 0.102% 0.114% 0.041% 1.642%

2-Moderate Injury 4.683% 0.398% 0.337% 0.399% 1.009%

3-Serious Injury 5.729% 0.290% 0.102% 3.111%

4-Severe Injury 5.884% 0.316% 0% 3.647%

5- Critical Injury 20.646% 20.646%
22

Table 15. Short-Term Household Production Loss and Percentage of Lifetime Household 

Production Lost to Traumatic Brain Injury by Abbreviated Injury Scale (AIS) Threat to Life 

Severity 

AIS Admitted ED & Released Outpatient Dept MD Office All

Short-Term Household Production Lost (in 2000 dollars)

1 $732 $249 $94 $96 $275

2 $678 $162 $101 $137 $232

3 $1,186 $400 $113 $780

4 $1,033 $158 $49 $681

5 $1,009 $1,009

Percentage of Lifetime Household Production Lost

1 7.081% 0.096% 0.093% 0.083% 1.725%

2 4.775% 0.445% 0.500% 0.483% 1.068%

3 5.689% 0.373% 0.061% 3.117%

4 6.716% 0.281% 0.024% 4.132%

5 19.238% 19.238%
23

Quality of Life Loss 

This section reviews existing evidence on quality of life loss, willingness to award 

compensation for, and willingness to pay to reduce the risk of CO and lead poisoning and 

submersion. It relies primarily on existing quality-adjusted life year (QALY) rating scales to 

quantify quality of life loss. A QALY is a health outcome measure defined such that a year in 

perfect health is 1, death is 0, and fates worse than death are allowed. Most Americans and 

Canadians rate a persistent unconscious state as worse than death (see, e.g., the systematic 

review in Miller et al., 1995).

One family of QALY rating scales proved especially applicable to the health conditions 

under study. Versions 1 and 2 of the Health Utility Index (HUI) were designed to assess QALY 

loss associated with birth-related problems and chronic childhood conditions (Torrance et al. 

1982, 1996). Torrance et al. (1982, 1996) surveyed 112 Ontario parents to calibrate HUI-1 and 

194 to calibrate HUI-2. HUI-1 estimates 20 percent QALY loss is associated with needing 

special education due to trouble learning or remembering. QALY loss rises to 48 percent if the 

condition will make it impossible for the child to work in a normal setting and 81 percent if the 

child also will need long-term help with self-care (eating, dressing, bathing, toileting). 

Torrance et al. (1996) consider HUI-2 a refinement of HUI-1. It assesses more cognitive 

and self-care states but does not address work-readiness. Table 16 shows HUI-2 scores for the 

range of health states commonly associated with CO poisoning, lead poisoning, and submersion.

The mildest retardation causes a 5 percent lifetime QALY loss, with retardation serious enough 

to require special education associated with a 13 percent loss and severe retardation a 51 percent

loss. Because lead poisoning harms reproductive health, it adds a further 2 percent to 3 percent

loss. Blood lead levels above 60 μg/dL create habitual irritability, which raises losses by 15

percent to 30 percent. Both CO poisoning and submersion can impair hearing. Depending on 

degree of hearing loss and severity of retardation, a further 15 percent to 30 percent loss of 

lifetime QALYs results. The limitation of these estimates is that frequency data on these health 

status changes do not exist.

Several studies focus more narrowly on retardation losses. Miller (2004) reviewed QALY 

loss estimates related to reduced IQ loss and retardation. Table 17 summarizes its estimates. 

They tend to be higher than the estimates in Table 16, with maximum loss exceeding 80 percent. 
24

Table 16. Health Utility Index 2 Estimates of Utility Loss for Brain Injury by Functional Impact 

Normal 

self-care

Independent selfcare with difficultyNeeds help to eat, 

bathe, dress, or toilet

With No Impact on Mobility, 

Emotional Health, Pain, or 

Reproductive Health

Learns and remembers more slowly than

classmates 5.3% 8.3% 25.4%

Requires special education because learns 

and remembers very slowly 12.7% 15.5% 31.4%

Unable to learn and remember 37.1% 39.2% 50.9%

With Mild Impact on Reproductive 

Health (any positive lead level)

Normal 

self-care

Independent selfcare with difficultyNeeds help to eat, 

bathe, dress, or toilet

Learns and remembers more slowly than 

classmates 8.3% 11.3% 27.9%

Requires special education because learns 

and remembers very slowly 15.5% 18.2% 33.6%

Unable to learn and remember 39.2% 41.2% 52.5%

With Habitual Irritability (BLL>=60 

μg/dL) + Reproductive Impact

Normal 

self-care

Independent selfcare with difficultyNeeds help to eat, 

bathe, dress, or toilet

Learns and remembers more slowly than 

classmates 37.6% 39.7% 51.3%

Requires special education because learns 

& remembers very slowly 42.7% 44.6% 55.3%

Unable to learn and remember 59.2% 60.6% 68.6%

With Hearing Limitations (possible 

sequelae, submersion or CO poisoning)

Normal 

self-care

Independent selfcare with difficultyNeeds help to eat, 

bathe, dress, or toilet

Learns and remembers normally 14.8% 17.6% 33.1%

Learns and remembers more slowly than 

classmates 19.4% 22.0% 36.7%

Requires special education because learns 

and remembers very slowly 25.8% 28.2% 41.8%

Unable to learn and remember 46.7% 48.5% 58.6%

With Deafness (possible sequelae, 

submersion or CO poisoning)

Normal 

self-care

Independent selfcare with difficultyNeeds help to eat, 

bathe, dress, or toilet

Learns and remembers normally 41.3% 43.3% 54.3%

Learns and remembers more slowly than 

classmates 44.6% 46.4% 56.9%

Requires special education because learns 

and remembers very slowly 49.1% 50.8% 60.5%

Unable to learn and remember 64.0% 65.2% 72.4%

Computed with the Torrance et al. (1996) scoring algorithm. 
25

Table 17. Utility Loss Associated with Retardation 

Condition % Utility Loss Source

Very severely 

retarded

83

75+

91

Torrance (1996)

Am Med Assoc. (1984)

MacKenzie (1994)

Retarded, needing 

help with care

57

54–57

55–75

77

Kaplan (1976)

Torrance (1996)

Am Med Assoc. (1984)

MacKenzie (1994)

Moderately retarded 

with self-care

42–51

48–51

25–50

49

Kaplan (1976)

Torrance (1996)

Am Med Assoc. (1984)

MacKenzie (1994)

Mildly retarded 33

20–27

23

23

10–20

26

Kaplan (1976)

Torrance (1996)

Sintonen (1994)

Glotzer (1995)

Am Med Assoc. (1984) 

MacKenzie (1994)

Source: Miller et al. (2004) 

In Global Burden of Disease studies (World Health Organization (WHO) 2008), Dutch 

EQ-5d survey data indicated mild mental retardation attributable to lead exposure results in a 

36.1 percent QALY loss. This estimate is lower than WHO’s earlier 45.9 percent loss estimate 

for mental retardation, which was based on expert judgment (World Health Organization, 2008). 

It is consistent with moderate retardation estimates in Table 17 but higher than the HUI-2 

estimates in Table 16.

EPA took a jury verdict approach to value the quality of life loss associated with 

developmental toxicity (Lopez et al. 1995). From 132 jury verdicts for severe birth defects 

(cerebral palsy with severe mental retardation, quadriplegia, other symptoms that require lifetime 

custodial care, deafness, and blindness), they estimated willingness to award for a severe birth 

defect was $8.0 million (inflated to 2010 dollars) with a standard deviation of $7.6 million. That 

far exceeds other estimates. We also experimented with a jury verdict approach, using jury 

verdict data that CPSC purchased on near-drowning (9 cases) and nonfire-related carbon 

monoxide poisoning (92 cases). Unfortunately, virtually none of the cases stated past or future 

medical or earnings losses. Without data on these monetary losses, which are included in the 

compensation paid, it was impossible to develop a regression equation to estimate non-monetary 
26

losses from monetary losses. The data also included minimal information on victim heath status, 

with the large majority of cases merely coded as CO poisoning. Among the cases with diagnostic 

information, seven were coded as headaches, eight as mild brain damage, one as moderate brain 

damage, one as seizure disorders, one as paraplegia, and one as death. Circumstance data also 

were quite spotty, with most cases merely coded as accidents at different locations (e.g., rental 

homes, motels).

Torrance et al. (1982) also provides a basis for computing QALY loss from work loss for 

impairments like IQ loss that primarily impact earning capacity. Torrance estimates lost ability to 

work causes a 32.66 percent QALY loss. Applying that estimate in conjunction with the QALY 

valuation that CPSC’s ICM uses in its sensitivity analyses, monetized QALY loss from lost work 

is 1.43 times associated wage, fringe benefit, and household production losses, implying an 

incremental quality of life loss of 0.43 times productivity loss. 

Lead Poisoning 

Several studies estimated lifetime losses from lead poisoning directly. Agee and Crocker 

(1996) examined household decisions about obtaining chelation therapy for 256 lead-exposed 

children (with much higher exposures than currently are typical). They estimated willingness to 

pay (WTP) was $24 for a 1 percent reduction in a child’s lead burden, with a range from $16 for 

households that decided against chelation therapy to $155 for ones that chose it. WTP was 3.1 

times medical plus work losses a weighted average of ratios of 20.0 for those choosing chelation 

and 2.1 for those choosing against it. Perhaps because they are for high lead exposures, all three 

ratios (3.1, 20.0, and 2.1) exceed the all-cause ratio of 1.43 from Torrance et al. (1982). Lutter 

(2000) claimed to convert Agee and Crocker’s estimates into WTP of $1,100 to $1,900 per IQ 

point gained; his estimate that WTP is about 1/6 of the wage loss is inconsistent with Agee and 

Crocker’s underlying estimate and with Torrance’s estimate.

At current exposure levels, Muennig (2009), using 2000−2002 MEPS EQ5d data, 

estimated lifetime QALY loss per lead-exposed child averages 20 percent (computed at a 3 

percent discount rate, with standard deviation of 8 percent). That estimate is slightly above Table 

16 estimates, close to moderate retardation estimates in Table 17, and below the Dutch EQ5d 
27

estimate of 36 percent. We consider it the best estimate for lead poisoning, with sensitivity 

analysis recommended at 15 percent and 35 percent loss. 

CO Poisoning 

Without a CO alarm in a home, CO poisoning often continues for some time before it is 

detected. Table 18 shows the signs and symptoms that may accumulate prior to detection. 

Treatment with oxygen, either normobaric (face mask) or hyperbaric (high-pressure chamber) 

clears many of these symptoms, at least initially. Neurologic symptoms, however, often persist 

or develop days to weeks after apparent recovery. UHMS data indicate that 17.7 percent of those 

treated with hyperbaric oxygen who were tested (15.1 percent of all hyperbaric patients) had 

cardiac abnormalities consistent with cardiac injury. 

A randomized trial of hyperbaric oxygen treatment gives probabilities of longer term 

sequelae among 224 patients treated in emergency departments or admitted (Weaver et al. 2007, 

Weaver 2009). Initial carboxyhemoglobin levels in this population averaged 22 percent with a 

standard deviation of 11 percent. Those levels are greatly influenced by how long the victim was 

removed from the CO exposure and how long they received normobaric oxygen en route/at the 

treating facility. Hampson et al. (2012) reported initial levels for 1,394 hyperbaric patients 

averaged 23.4 percent with a standard deviation of 10.4 percent and a range from 0.1-77.0

percent. Their samples were obtained an average of 2.2 hours from the end of the CO exposure 

(standard deviation 6.9 hours, range 0 to 198 hours).

Table 18. Acute Symptoms in 1144 Patients with 

Carbon Monoxide Poisoning 

Symptom % of Patients

Headache 85%

Dizziness 69%

Fatigue or generalized weakness 67%

Nausea or vomiting 52%

Trouble thinking or confusion 37%

Loss of consciousness 35%

Dyspnea 7%

Chest pain 2%

Source: Lavonas, 2007, pooled data from 7 studies. 

Table 19 shows the probability of neurocognitive sequelae over time, with and without 

hyperbaric oxygen. Without hyperbaric oxygen, 34 percent of patients reported headaches at four
28

weeks (Weaver 2009). In a follow-up study, six years after poisoning, 37 percent (17/42) had 

abnormal neurologic evaluations, and 19 percent (10/52) had cognitive problems, with some 

unstated overlap (Weaver 2009). Of 17 patients with neurologic abnormalities, 88 percent had 

cerebellar, 29 percent cranial, 29 percent motor, 18 percent deep tendon reflex, and 12 sensory 

abnormalities (Weaver et al. 2008). Of 10 patients with cognitive deficits, all had deficits in 

visual memory, 80 percent in attention, 70 percent in verbal memory, and 70 percent in executive 

function in the Hopkins and Weaver abstracts for which no paper has been published (Hopkins & 

Weaver 2008). None had slow mental processing speed. 

Table 19. Probability of Neurocognitive Sequelae of Carbon Monoxide Poisoning 

by Treatment Mode and Time Post-Exposure 

No Oxygen Normobaric

Oxygen

Hyperbaric 

Oxygen

Sequelae at 6 weeks 53% (9/17) 41% (60/146) 24% (18/75)

At 6 Months 30% (44/146) 17% (10/58)

At 12 Months 18% (27/149 14% (9/62)

Source: Weaver et al., 2007 The source did not differentiate sequelae at 6-12 months between no oxygen 

and normobaric oxygen.

Delayed sequelae were common. Among 75 patients with neurocognitive sequelae who 

participated in early repeat testing, 68 percent had persistent losses over the first six weeks; 12

percent experienced declines from function immediately post-treatment during weeks 1−2; and 

another 20 percent experienced declines during weeks 3−6. Only 6 of 17 patients with 

abnormalities after six years had cognitive sequelae at six weeks and only seven did at 12 months 

(Hopkins & Weaver 2008). The Hopkins and Weaver abstracts seemed to suggest some of the 

symptom increase was unrelated to the CO poisoning, but it was unclear how much.

Procedure codes in HCUP were too coarse to provide rates of hyperbaric oxygen use 

versus oxygen administration by face mask. The 1,500 hyperbaric chamber cases in 2002, and

the 14,236 medically treated cases in 2006, suggest that perhaps 10 percent to 12 percent receive 

hyperbaric treatment. In the nonrandomized portion of Weaver’s three-state study, 37 percent of 

those without hyperbaric oxygen received no oxygen (Weaver, 2009) (All hyperbaric oxygen 

was randomly assigned, so the study provided no insight into its usage frequency.) Applying that 

ratio suggests 26 percent to 27 percent of CO patients get no oxygen therapy. Sequelae rates 

would average 43 percent at six weeks, 29 percent at six months, 17 percent at 12 months, and 

19 percent to 37 percent at six years. Severity of cognitive sequelae was quite large, an average 
29

score three standard deviations below the population norm on a battery of seven

neuropsychological tests: general orientation, digit span, Trail Making (Parts A and B), digitsymbol, block design, and story recall (Weaver et al. 2007). Unfortunately, we could not 

translate that severity into HUI-2 categories. Based on the estimates in Table 16, we 

conservatively suggest assuming a 15 percent QALY loss for those with sequelae, with 

sensitivity analysis at 20 percent and 35 percent. With the $5 million value of statistical life that 

CPSC uses, lifetime QALYs are valued at $4,062,185 ($5,000,000 to $937,815 in productivity 

losses from above), so a 15 percent loss would be valued at $609,328.

Submersion 

No data on submersion severity was available because HCUP procedure codes lacked 

sufficient detail to identify intubation or ICU usage. We suggest assuming that 90 percent of 

admitted cases will be tracheotomy-tube dependent with utility losses in the 90 percent range, 

with the rest experiencing losses of perhaps 20 percent to 25 percent. We assume non-admitted 

cases would suffer no sequelae. 

Future Research 

For submersions and CO poisoning, if Medicaid claims data were available, we would 

use discharge to inpatient rehabilitation or long-term care, intensive care unit use, and intubation 

procedure codes to infer the frequency of severe sequelae. Receipt of services like physical and 

speech therapy could be used to infer the frequency of more moderate sequelae.
30

Summary 

In summary, this report provides incidence data and a wide range of data on costs per case for 

CO and lead poisoning and submersion, by exposure severity. Those data will improve ICM 

estimates for these severe health challenges. 

Unfortunately, severity distribution data are unavailable, so we can only provide average figures 

by assuming a distribution. The easiest and least burdensome way to get accurate severity 

distributions for CO poisoning and submersion is to analyze Medicaid or possibly private health 

insurance claims files. In the interim, our best estimates are: 

 For CO poisoning, quality-adjusted life-year (QALY) loss and lifetime earnings loss are 

perhaps 15 percent per year with sequelae, with at least 20 percent of patients 

experiencing lifetime sequelae. That implies a 3 percent lifetime loss. 

 For lead poisoning, a 20 percent QALY loss is the average for child exposures, with 

losses rising with blood lead level. Lead poisoning also results in ADHD and crime that 

are costly and further reduce quality of life. 

 For submersion, perhaps 90 percent of hospital inpatients experience a 90 percent QALY 

loss, with the remainder experiencing losses of 20 percent to 25 percent, yielding a 

combined average of 83 percent. Treated and released cases probably experience minimal 

QALY loss. 
31

References 

Agarwal N. Economic Analysis of Toxic Substances Control Act Section 403 Hazard 

Standards, Washington, DC: Economic and Policy Analysis Branch, U.S. Environmental 

Protection Agency, 1998. 

Agee MD, Crocker TD. Parental altruism and child lead exposure: Inferences from the 

demand for chelation therapy, Journal of Human Resources, 31:3, 677−691, 1996. 

American Medical Association. Guides to the Evaluation of Permanent Impairment, 

Chicago IL, 1984. 

Braun JM, Kahn RS, Froehlich T, Auinger P, Lanphear BP (2006) Exposures to 

environmental toxicants and attention deficit hyperactivity disorder in US children. 

Environmental Health Perspectives, 114: 1904–1909, 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1764142/

Canfield RL, Henderson CR Jr, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP. 

Intellectual impairment in children with blood lead concentrations below 10 microgram per 

deciliter. New England Journal of Medicine, 348:16, 1517–1526, 2003.

CDC. Preventing lead exposure in young children: A housing-based approach to primary 

prevention of lead poisoning. Atlanta, GA: Centers for Disease Control and Prevention, 2004. 

CDC. Fourth national report on human exposure to environmental chemicals, updated 

tables, February 2012. Atlanta, GA: Centers for Disease Control and Prevention. 

http://www.cdc.gov/exposurereport/, 2012.

Chambers JG, Shkolnik J, Pérez M. Total Expenditures for Students with Disabilities, 

1999-2000: Spending Variation by Disability. Report 5, Special Education Expenditure Project, 

Washington DC: American Institutes for Research, 2003. 

Chandramouli K, Steer CD, Ellis M, Emond AM. Effects of early childhood lead 

exposure on academic performance and behaviour of school age children. Archives of Disease in 

Childhood, 94:11, 844-848, 2009. 

Chen A, Cai B, Dietrich KN, Radcliffe J, Rogan WJ. Lead exposure, IQ, and behavior in 

urban 5- to 7-year-olds: Does lead affect behavior only by lowering IQ? Pediatrics, 119, 

e650−e658, 2007. 

Coghill D, Spender Q, Barton J, Hollis C, Yuen C, Cleemput I, et al. Measuring quality 

of life in children with attention-deficit-hyperactivity-disorder in the United Kingdom. In: 16th 

World Congress of the International Association of Child and Adolescent Psychiatry and Allied 

Professions (IACAPAP); 2004 Aug 23−26; Berlin, Germany. 2004. 

CPSC. Staff Report: CPSIA Section 101(b): Functional purpose exception from lead 

content limit for children’s products for a specific product, class of product, material, or 

component part. U.S. Consumer Product Safety Commission. 

http://www.cpsc.gov/PageFiles/133902/lead101.pdf, 2012. 

Dietrich KN, Ware JH, Salganik M, Radcliffe J, Rogan WJ, Rhoads GG, Fay ME, Davoli 

CT, Denckla MB, Bornschein RL, Schwarz D, Dockery DW, Adubato S, Jones RL. Effect of 
32

chelation therapy on the neuropsychological and behavioral development of lead-exposed 

children after school entry. Pediatrics, 114:1, 19−26, 2004. 

EPA. Air quality criteria for lead. Final report. U.S. Environmental Protection Agency. 

EPA/600/R-05/144aF-bF, http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=158823 , 2006. 

Gilmore A, Milne R: Methylphenidate in children with hyperactivity: review and costutility analysis. Pharmacoepidemiology Drug Safety , 10:85−94, 2001. 

Gipson K. Pool or spa submersion: estimated injuries and reported fatalities, 2011 report. 

Bethesda, MD: CPSC, 2011a. 

Gipson K. Submersion related to non-pool and non-spa products, 2011 report. Bethesda, 

MD: CPSC, 2011b. 

Glotzer DE, Freedberg KA, Bauchner H. Management of childhood lead poisoning: 

Clinical impact and cost-effectiveness, Medical Decision Making 15:1, 13−24, 1995. 

Gould E. Childhood lead poisoning: Conservative estimates of the social and economic 

benefits of lead hazard control. Environmental Health Perspectives, 117, 1162–1167, 2009. 

Grosse SD., Matte TD, Schwartz J, Jackson RJ. Economic gains resulting from the 

reduction in children's exposure to lead in the United States. Environmental Health Perspectives, 

110:6, 563−569, 2002. 

Hampson NB, Little CE. Hyperbaric treatment of patients with carbon monoxide 

poisoning in the United States. Undersea and Hyperbaric Medicine, 32:1, 21−26, 2005. 

Hampson NB, Rudd RA, Hauff NM. Increased long-term mortality among survivors of 

acute carbon monoxide poisoning. Critical Care Medicine, 37:6, 1941−1947, 2009. 

Hampson NB, Dunn SL, Yip FY, Clower JH, Weaver LK. The UHMS/CDC carbon 

monoxide poisoning surveillance program three-year data. Undersea and Hyperbaric Medicine, 

39:2, 667-685, 2012.

Hnatov M. Nonfire carbon monoxide deaths associated with the use of consumer 

products: 2009 estimates. Bethesda, MD: CPSC, 2012. 

Hopkins, RO; Weaver, LK . Cognitive outcomes 6 years after acute carbon monoxide 

poisoning. Abstract of the Undersea & Hyperbaric Medical Society 2008 Annual Scientific 

Meeting, http://archive.rubicon-foundation.org/7822, 2008. 

Jones RL, Homa DM, Meyer PA, Brody DJ, Caldwell KL, Pirkle JL, Brown MJ. Trends 

in blood lead levels and blood lead testing among US children aged 1 to 5 years, 1988–2004. 

Pediatrics, 123:3, e376−e385, 2009. 

Kaplan RM, Bush JW, Berry CC. Health status: Types of validity for an index of wellbeing. Health Services Research 11(4):478-507, 1976. 

Keogh JP, Boyer LV: Lead. In Sullivan JB, Krieger GR (eds): Hazardous Materials 

Toxicology, 2nd ed. Baltimore: Williams & Wilkins, 879−889, 2001. 

Lanphear BP, Hornung R, Khoury J, Yolton K, Baghurst P, Bellinger DC, Canfield RL, 

Dietrich K, Bornschein R, Greene T, Rothenberg SJ, Needleman HL, Schnaas L, Wasserman G, 
33

Graziano J, Roberts R. Low-level environmental lead exposure and children’s intellectual 

function: An international pooled analysis, Environmental Health Perspectives, 113,894–899, 

2005.

Laosee OC, Gilchrist J, Rudd RA. Drowning—United States, 2005–2009. Morbidity and 

Mortality Weekly Report, 61:19, 344−347, 2012. 

Lavonas EJ. Carbon monoxide poisoning. In Shannon MW, Borron SW, Burns M [Eds.], 

Haddad and Winchester’s Clinical Management of Poisoning and Drug Overdose, 4th ed. 

Philadelphia: Elsevier, 1297−1307, 2007. 

Lopez A, Dexter RN, Reinert JC. Valuation of developmental toxicity outcomes. The 

Environmental Professional, 17, 186-192, 1995. 

Lutter R. Valuing children's health: A reassessment of the benefits of lower lead levels, 

Working Paper No. 00-02, Washington DC: American Enterprise Institute-Brookings Joint 

Center for Regulatory Studies, 2000. 

MacKenzie E, Miller TR. The development of the functional capacity index. NHTSA, 

1994.

Miller TR. The social costs of problem behavior. Chapter 3 in Biglan A, Brennan PA, 

Foster SL, Holder HD, Miller TR, Cunningham PB, Derzon JH, Fishbein DH, Flay BR, Goeders 

NE, Kelder SH, Kenkel D, Meyer R, Zucker RA. The social costs of problem behavior. Helping 

adolescents at risk: Prevention of multiple problem behaviors. New York: Guilford Press, 31−56, 

2004.

Miller TR. Valuing non-fatal quality of life losses with quality-adjusted life years: The 

health economist's meow, Journal of Forensic Economics, 13:2, 145−168, 2000.

Miller TR, Hendrie D. Costs of criminal victimization, United States, 2010. Woring 

Paper. Calverton MD: Pacific Institute for Research & Evaluation, 2013. 

Miller TR, Pindus NM, Douglass JB, Rossman SB. Databook on nonfatal injury – 

Incidence, costs, and consequences, Washington DC: The Urban Institute Press, 1995.

Miller TR, Zaloshnja E, Hendrie D. The cost of traumatic brain injuries and the return on 

helmet investment in the United States. In J Jallo, C Loftus (ed.), Neurotrauma and Critical Care 

of the Brain, New York: Thieme, 445-459, 2009. 

Muennig P. The social costs of childhood lead exposure in the post–lead regulation era. 

Archives of Pediatric and Adolescent Medicine, 163:9, 844−849, 2009. 

Nahin RL, Barnes PM, Stussman BJ, Bloom B. Costs of complementary and alternative 

medicine (CAM) and frequency of visits to CAM practitioners: United States, 2007. National 

Health Statistics Reports; no 18. Hyattsville, MD: National Center for Health Statistics. 2009. 

National Center for Education Statistics, Digest of Education Statistics 2011, 

http://nces.ed.gov/programs/digest/d10/tables/dt10_190.asp

Neal DA, Johnson WR. The role of premarket factors in black-white wage differences. 

Journal of Political Economy, 104, 869-895, 1996. 

Needleman HL. Lead poisoning. Annual Review of Medicine, 55, 209–222, 2004. 
34

Office of Inspector General. Hyperbaric oxygen therapy: Its use and appropriateness, OEI 

06-99-00090, Dallas Regional Office, Department of Health and Human Services, 2000. 

Pocock SJ, Smith M, Baghurst P. Environmental lead and children’s intelligence: a 

systematic review of the epidemiological evidence. British Medical Journal, 309:1189–1197, 

1994.

Salkever, DS. Updated estimates of earning benefits from reduced exposure of children to 

environmental lead. Environmental Research. 70, 1-6, 1995. 

Schwartz J. Low-level lead exposure and children’s IQ: a meta-analysis and search for a 

threshold. Environmental Research, 65:1, 42–55, 1994a. 

Schwartz J. Societal benefits of reducing lead exposure. Environmental Research, 66:1, 

105–124, 1994b. 

Secnik K, Matza LS, Cottrell S, Edgell E, Tilden D, Mannix S. Health state utilities for 

childhood attention-deficit/hyperactivity disorder based on parent preferences in the United 

Kingdom, Medical Decision Making, 25, 56−70, 2005. 

Sintonen H. The 15D-measure of health-related quality of life. I. Reliability, validity and 

sensitivity of its health state descriptive system. Working Paper 41. Melbourne, Vict: National 

Centre for Health Program Evaluation, 1994.

Swanson CB, Bausell CV, Delgado R, Dorko K, Lloyd S, Miller P, Mitani H.. Special 

Education in America. Bethesda MD: Editorial Projects in Education Research Center, 2008. 

Swensen A, Birnbaum HG, Secnik K, Marynchenko M, Greenberg P, Claxton A. 

Attention-deficit/ hyperactivity disorder: increased costs for patients and their families. Journal 

of the American Academy of Child and Adolescent Psychiatry 42:12, 1415−1423, 2003. 

Torrance GW. Multiattribute utility theory as a method of measuring social preferences 

for health states in long term care. In: Kane RL, Kane RM, eds. Values and Long-Term Care. 

Lexington: DC Heath, 127−156, 1982.

Torrance GW, Feeny DH, Furlong WJ, Barr RD, Zhang Y, Wang QA. Multi-attribute 

utility function for a comprehensive health status classification system: Health Utilities Index 

Mark 2. Medical Care. 34:7, 702–722, 1996.

Weaver, LK; Hopkins, RO; Churchill, S; Chan, KJ. Randomized trial carbon monoxide 

poisoned patients compared to nonrandomized patients. Abstract of the Undersea & Hyperbaric 

Medical Society 2008 Annual Scientific Meeting, http://archive.rubicon-foundation.org/1358,

2003.

Weaver LK, Valentine KJ, Hopkins RO. Carbon monoxide poisoning: risk factors for 

cognitive sequelae and the role of hyperbaric oxygen. American Journal of Respiratory Critical 

Care Medicine, 176, 491−497, 2007. 

Weaver, LK; Hopkins, RO; Churchill, SK; Deru, K. Neurological outcomes 6 years after 

acute carbon monoxide poisoning. Abstract of the Undersea & Hyperbaric Medical Society 2008 

Annual Scientific Meeting, http://archive.rubicon-foundation.org/7823, 2008.
35

Weaver LK. Carbon monoxide poisoning. New England Journal of Medicine, 360: 12, 

1217−1225, 2009.

World Health Organization. The global burden of disease, 2004 update. Geneva: WHO, 

http://www.who.int/healthinfo/global 

Wright JP, Dietrich KN, Ris MD, Hornung RW, Wessel SD, Lanphear BP, Ho M, Rae 

MN. Association of prenatal and childhood blood lead concentrations with criminal arrests in 

early adulthood. PLOS Medicine, 5:5, e101, 732−740, 2008. 

Zaloshnja, E., Miller, T., Jones, P., Litovitz, T., Coben, J., Steiner, C., & Sheppard, M. 

(2008). The impact of poison control centers on poisoning-related visits to emergency 

departments, U.S., American Journal of Emergency Medicine, 26:3, 310−315. 

Zamula W. Social costs of drownings and near-drownings from submersion accidents 

occurring to children under 5 in residential swimming pools, Bethesda MD: Directorate for 

Economic Analysis, 1987.
36

Appendix A: Other Costs of Lead Poisoning 

Special Education. EPA analyzed the costs of special education for children with leadinduced IQ deficits (Agarwal, 1998). We used their estimates of the frequency of special 

education usage and updated associated costs with current data from the U.S. Department of 

Education. “The number of children with IQ less than 70 and the number of children with blood 

lead levels above 20 μg/dL can be used to measure cognitive effects seen mostly in children with 

high levels of lead exposure. An IQ score of 70 is two standard deviations below the population 

mean; it is used as an indicator of mental retardation and as the cut-off for special education 

requirements. Blood lead levels above 20 μg/dL are the level at which CDC traditionally 

recommended complete medical evaluation, environmental assessment, and necessary 

environmental remediation for the child and his/her environment. EPA (Agarwal, 1998) used 

NHANES III data to indicate the fraction of one to two-year olds falling within these categories. 

An estimated 0.115% of children with lead poisoning have IQs under 70 as a result, and 0.588%

have blood lead levels above 20 μg/dL.” (Agarwal, 1998). These data suggest that 19.6% 

(.115/.588) of children with lead levels exceeding 20 μg/dL require special education.

Exclusive of capital spending and debt service, average spending per pupil in U.S. public 

elementary or secondary school was $10,441 in FY 2007−2008 (National Center for Education 

Statistics, 2011, Table 190, in Feb 2009 dollars).2 Based on a massive national study, Chambers 

et al. (2003) reports that spending per special education student is 1.6 times spending on other 

students. Swanson (2008) reports that 9 percent of U.S. students have special educational needs. 

Thus the additional spending per US special needs student is $5,944 (0.6 * $10,441 / (.91 + .09 * 

1.6)). The special education multipliers average (a) 2.3 for mental retardation (or for orthopedic 

impairment) and (b) 2.5 for traumatic brain injury (Chambers et al. 2003, Exhibit 1), implying 

annual special education costs of (a) $22,784 and (b) $24,765 for these conditions. Thus special 

education spending per lead poisoning case at ages 0-4 averages $4,660 per school year or 

$46,713 in present value from grades K−12 (assuming exposure at age 2). 

 

2

 This estimate excludes $1,676 per pupil in annual capital spending and debt service. Those costs would not be 

higher for special education students. 
37

ADHD. Braun et al. (2006) analyzed data from the National Health and Nutrition 

Examination Survey (NHANES-III) and found that children with blood lead concentrations 

greater than 2 μg/dl were at a 4.1-fold increased risk of ADHD. Medical costs of ADHD average 

$1,586 per year (or $14,984 from ages 6 through 18, brought to present value using a 3 percent 

discount rate; inflated to 2009 dollars) (Swensen et al., 2003). This estimate is based on cost 

differentials relative to a matched control group in a privately insured population. The present 

value of QALY losses through age 18 for ADHD diagnosed at age 6 averages 1.9. Secnik et al. 

(2005) estimated the mean QALY level for a child with an acute case of ADHD at 0.74. They 

rated the utility of someone with chronic ADHD treated with no side effects at 0.96 compared to 

unmedicated utility of 0.88, implying an annual utility loss of at least 0.08 and possibly as much 

as 0.12 from chronic ADHD. These estimates were based on children in the United Kingdom 

assessed using the EQ5d QALY instrument. Data were not readily available on the QALY norm 

for the age group studied. No comparable United States data were available. Coghill et al. (2004) 

estimated utility of an ADHD responder to treatment at 0.837 (standard error 0.039) and of a 

non-responder to treatment at 0.773 (standard error 0.039), independent of treatment received, 

suggesting a loss of at least 0.064 (0.837–0.773).

Crime. Wright et al. (2008) finds that child lead poisoning increases criminal behavior. 

“Adjusted total arrest rates” for violent and non-violent crime “at ages 18−24 were greater for 

each 5 μg/dl increase in blood lead concentration:” Relative risk (RR) “ = 1.07 (95% CI 0.88–

1.29) for average childhood blood lead through age 6, and 1.27 (95% CI 1.03–1.57) for blood 

lead at age 6. Adjusted arrest rates for violent crimes at ages 18−24 were greater for each 5 μg/dl 

increase in blood lead: RR = 1.30 (95% CI 1.03–1.64) for average childhood blood lead, and 

1.48 (95% CI 1.15–1.89) for blood lead at age 6.” We assume these odds ratios apply to both 

youth and subsequent adult crime, and that the differential arrest rates match the differential 

crime rates. If lead poisoning is relatively rare, with RR=1.27, per 5 μg/dl, crime associated with 

lead poisoning will equal roughly 0.27 times the average crime rate. With crime incidence from 

Miller and Hendrie (2013), RR for non-violent crime would be 1.23 (0.27 * 98,827,502 crimes -

0.48 * 20,380,407 violent crimes)/ 78,447,095 non-violent crimes) for each 5 μg/dl increase in 

blood lead.
38

Using these RRs requires separate costs for violent and non-violent personal crimes 

covered in arrest data. We relied on estimates from Miller and Hendrie (2013), but substituted 

the $5 million value of a statistical life that CPSC uses in its regulatory analyses. 

Table 20 summarizes unit costs by crime used to estimate costs per crime. Table 21 

presents incidence, percentage of crimes reported to police, and percentage leading to arrest. 

Costs per police-reported crime averaged $49,727 for violent crime and $3,328 for property 

crime. Costs per crime were lower at ages 8−18 than at ages 18 and older. 

Table 22 shows the age distribution of arrestees and associated crimes per person under 

the assumption that virtually all arrests at ages 0−14 occur at ages 8−14. Applying the rise in 

relative risk from above to the crime rate per capita, then multiplying times cost per crime yields 

the annual crime costs per 5 μg/dl rise in blood lead level by age shown in the right-hand 

columns. We computed present value of these annual costs over a lifespan starting at age 2, 

accounting for life table probabilities of survival from year to year. Conservatively, except in 

sensitivity analysis, we restricted Table 22 to police-reported crimes and excluded impaired 

driving crashes, intimate partner violence, and child maltreatment. Present value of estimated 

costs per 5 μg/dl rise in blood lead level are $77,125, including $74,898 in violent crime costs 

and $2,228 in non-violent crime costs. Had we assumed crimes not reported to the police are 

reduced proportionately to police-reported crimes and included all personal crimes, estimated 

crime costs per 5 μg/dl rise in blood lead level would be $181,824, including $176,516 in violent 

crime costs and $5,308 in non-violent crime costs. 

Blood lead level elevation from consumer products depends on method and duration of 

exposure. Licking a toy regularly, swallowing something, or licking a product on a single access 

are quite different exposures. To estimate resulting blood lead levels, a regulatory analysis 

presumably would draw on medical or engineering expertise or on historical data on elevation 

with similar exposures. 
39

Table 20. Costs per Police-Reported Crime by Cost Category in 2010 Dollars 

Medical Mental 

Health

Work Property 

Damage

Public 

Services*

Quality of 

Life

Adjudication & 

Sanctioning

Perpetrator 

Work Loss

Total

Murder $16,183 $10,735 $1,577,758 $175 $2,852 $3,422,242 $368,336 $143,023 $5,541,304

Rape $2,887 $5,830 $5,765 $157 $790 $128,196 $24,679 $9,517 $177,821

Robbery $1,313 $176 $2,716 $1,143 $405 $14,754 $11,866 $4,413 $36,786

Assault $1,141 $361 $1,879 $70 $335 $12,708 $5,655 $1,878 $24,027

Burglary $0 $0 $34 $2,564 $450 $0 $2,041 $693 $5,782

Larceny/Theft $0 $0 $27 $936 $442 $0 $778 $168 $2,351

Motor Vehicle Theft $0 $0 $102 $6,423 $269 $0 $1,778 $571 $9,143

Arson $2,373 $40 $2,924 $17,411 $3,561 $5,548 $2,310 $603 $34,770

Forgery/Counterfeiting $0 $0 $0 $414 $266 $0 $2,525 $682 $3,887

Person-to-Person Fraud $0 $0 $0 $1,687 $65 $0 $2,289 $682 $4,723

Embezzlement $0 $0 $0 $414 $266 $0 $2,743 $682 $4,105

Buying Stolen Property, $0 $0 $0 $0 $266 $0 $4,791 $1,169 $6,226

Vandalism $0 $0 $88 $261 $70 $0 $2,075 $724 $3,218

Weapons Carrying, $0 $0 $0 $0 $70 $0 $2,289 $799 $3,158

Prostitution/Pandering $0 $0 $0 $0 $70 $0 $229 $80 $379

Other Sex Offenses $1,278 $3,682 $3,947 $145 $316 $86,102 $24,679 $9,517 $129,666

Drug Possession/Sales $0 $0 $0 $0 $4,490 $0 $3,202 $1,118 $8,810

Gambling $0 $0 $0 $0 $70 $0 $229 $80 $379

DUI, No Crash $0 $0 $0 $0 $19 $0 $415 $145 $579

Liquor Law Violations $0 $0 $0 $0 $70 $0 $1,093 $381 $1,544

Drunkenness $0 $0 $0 $0 $70 $0 $1,093 $381 $1,544

Disorderly Conduct $0 $0 $0 $0 $70 $0 $1,093 $381 $1,544

Vagrancy $0 $0 $0 $0 $70 $0 $1,093 $381 $1,544

Curfew/Loitering Violations $0 $0 $0 $0 $70 $0 $1,093 $381 $1,544

All Other Nontraffic Offenses $0 $0 $0 $0 $70 $0 $229 $92 $391

All Violent Crime $1,254 $619 $7,016 $377 $396 $28,681 $8,410 $2,974 $49,727

All Other Personal Crime $0 $0 $27 $856 $622 $0 $1,386 $436 $3,328

Perpetrator Ages 8−17 Years

 All Violent Crime $1,202 $475 $3,358 $452 $403 $18,215 $6,855 $2,359 $33,320

 All Other Personal Crime $0 $0 $39 $969 $489 $0 $1,425 $449 $3,371

Perpetrator Ages 18 & Over

 All Violent Crime $1,280 $691 $8,835 $340 $392 $33,885 $9,183 $3,280 $57,885

 All Other Personal Crime $0 $0 $24 $831 $652 $0 $1,405 $444 $3,356

* Public services include police, fire, EMS, victim services. Violent crimes are rape, robbery, assault, arson, other sexual offenses, intimate partner violence, and child 

maltreatment. 
40

Table 21. Percentage of Crimes Reported, Percentage of Reported Crimes that Lead to 

an Arrest, and Number of Arrests in 2010 

Reported 

Crimes

% 

Reported

% Arrested 

of Reported

% Under 

Age 18 Arrests

Murder 16,259 100.0% 73.9% 9.0% 11,201

Rape 92,322 9.8% 21.8% 14.1% 20,088

Robbery 409,584 65.6% 27.4% 24.1% 112,300

Assault 4,414,537 43.8% 38.1% 15.4% 1,700,937

Burglary 2,385,971 50.7% 12.1% 22.7% 289,769

Larceny/Theft 8,460,936 31.0% 15.0% 22.3% 1,271,410

Motor Vehicle Theft 761,669 85.4% 9.4% 22.1% 71,487

Arson 65,763 100.0% 20.4% 48.5% 13,416

Forgery/Counterfeiting 293,828 31.0% 26.6% 2.2% 78,101

Fraud 1,166,474 31.0% 16.1% 3.2% 187,887

Embezzlement 46,681 31.0% 35.6% 2.7% 16,616

Buying Stolen Property, 157,806 100.0% 60.1% 15.6% 94,802

Vandalism 3,594,637 8.3% 7.0% 30.6% 252,753

Weapons Carrying, 322,300 100.0% 49.3% 19.8% 159,020

Prostitution 66,926 100.0% 93.6% 1.7% 62,668

Other Sex Offenses 232,953 9.8% 31.2% 18.0% 72,628

Drug Possession/Sales 2,242,480 100.0% 73.1% 10.4% 1,638,846

Gambling 11,458 100.0% 86.8% 13.8% 9,941

Intimate Partner Violence 628,331 3.7% 100.0% 3.5% 111,062

Child Maltreatment 512,790 22.9% 100.0% 6.0% 689,435

Driving Under the Influence 560,718 31.2% 100.0% 0.9% 1,412,223

Liquor laws 615,172 100.0% 100.0% 18.9% 512,790

Drunkenness 32,033 100.0% 100.0% 2.3% 560,718

Disorderly conduct 94,797 100.0% 100.0% 25.1% 615,172

Vagrancy 3,720,402 100.0% 100.0% 6.8% 32,033

Curfew/Loitering Violations 5,231,417 100.0% 100.0% 100.0% 94,797

All Other Non-Traffic Offenses 25,675,409 100.0% 100.0% 8.0% 3,720,402

All Violent Crimes 16,259 27.9% 48.5% 14.8% 2,731,067

All Non-Violent Crimes 92,322 33.8% 25.0% 12.2% 512,790
41

Table 22. Annual Arrest Rate and Estimated Crimes Committed per Person by Age Range, 2010, 

and Estimated Annual Violent and Property Crime Costs Over Different Age Ranges per 5 μg/dl 

Rise in Blood Lead Level at Age 0−4 (in 2010 dollars) 

Age Group

% 

Arrested

PoliceReported 

Crimes 

per Person

Police-Reported Only; No 

DWI, Domestic Violence All Crime

Violent 

Crime Cost

Property 

Crime Cost

Violent 

Crime Cost

Property 

Crime Cost

8 to 14 years 1.14% 0.045 $1,041 $31 $1,919 $41

15 to 19 years 8.68% 0.342 $7,918 $235 $14,600 $313

20 to 24 years 9.45% 0.218 $5,640 $168 $15,276 $521

25 to 29 years 7.18% 0.166 $4,285 $128 $11,605 $396

30 to 34 years 5.57% 0.129 $3,324 $99 $9,004 $307

35 to 39 years 4.33% 0.100 $2,582 $77 $6,995 $239

40 to 44 years 3.79% 0.087 $2,261 $67 $6,124 $209

45 to 49 years 3.16% 0.073 $1,887 $56 $5,112 $174

50 to 54 years 2.15% 0.050 $1,285 $38 $3,482 $119

55 to 59 years 1.23% 0.028 $732 $22 $1,983 $68

60 to 64 years 0.64% 0.015 $382 $11 $1,034 $35

65 years & over 0.19% 0.004 $111 $3 $302 $10

Arrest rates from Table 4.4, Sourcebook of Criminal Justice Statistics 2010. Washington DC: Bureau of Justice 

Statistics, 2012. 
42

Appendix B: Narrative Descriptors for 

International Classification of Disease Codes and 

NEISS Codes Included 

Codes from the 9th Edition of ICD, Clinical Modification, 

http://www.cdc.gov/nchs/icd/icd9cm.htm 

984 Toxic effects of lead and its compounds (including fumes) 

986 Toxic effect of carbon monoxide 

994.1 Drowning and nonfatal submersion 

E830 Accident to watercraft causing submersion 

E832 Other accidental submersion or drowning in water transport accident 

E861.5 Accidental poisoning by lead paints 

E866.0 Accidental poisoning by lead and its compounds and fumes 

E868 Accidental poisoning by other utility gas and other carbon monoxide 

E868.0 Liquefied petroleum gas distributed in mobile containers 

 Butane or carbon monoxide from incomplete combustion of these gases 

Liquefied hydrocarbon gas NOS or carbon monoxide from incomplete 

combustion of these gases 

 Propane or carbon monoxide from incomplete combustion of these gases 

E868.1 Other and unspecified utility gas 

 Acetylene or carbon monoxide from incomplete combustion of these gases 

Gas NOS used for lighting, heating, or cooking or carbon monoxide from 

incomplete combustion of these gases 

 Water gas or carbon monoxide from incomplete combustion of these gases 

E868.2 Accidental poisoning by motor vehicle exhaust gas 

E868.3 Accidental poisoning by carbon monoxide from incomplete combustion of other 

domestic fuels 

E868.8 Accidental poisoning by carbon monoxide from other sources 

E868.9 Accidental poisoning by unspecified carbon monoxide 

E910 Accidental drowning and submersion 

Codes from the 10th Edition of ICD, 

http://apps.who.int/classifications/icd10/browse/2010/en (regardless of medical treatment, 

multiple cause of death data typically include both a diagnosis code and an external cause 

code) 

Diagnosis Codes 

T56.0 Toxic effect of lead and its compounds 

T58 Toxic effect of carbon monoxide 
43

External Cause Codes 

W 16 Diving or jumping into water causing injury other than drowning or submersion 

W 29 Contact with other powered hand tools and household machinery (washing 

machines) 

W65 Drowning and submersion while in bath-tub 

W66 Drowning and submersion following fall into bath-tub 

W67 Drowning and submersion while in swimming-pool 

W68 Drowning and submersion following fall into swimming-pool 

W73 Other specified drowning and submersion 

W74 Unspecified drowning and submersion 

X47 Accidental poisoning by and exposure to other gases and vapors 

Y17 Poisoning by and exposure to other gases and vapors, undetermined intent 

Y21 Drowning and submersion, undetermined intent 

NEISS Codes 

64 Submersion (including drowning)