Workers' Exposures to n-Propyl Bromide at an Aerospace

Components Manufacturer

Kevin W. Hanley, MSPH, CIH, REHS/RS

Kevin Dunn

Ron Sollberger

Industrywide Studies Branch

Division of Surveillance~Hazard Evaluations and Field Studies

National Institute for Occupational Safety and Health

Centers for Disease Control and Prevention

US Public Health Service

Department ofHealth and Human Services

IWSB 232.12

November 2006
Abstract

The National Institute for Occupational Safety and Health (NIOSH) conducted a field study at an

aerospace component manufacturing plant where n-propyl bromide (nPB) was used as a vapor

degreasing solvent. Workers' breathing zone and exhaled breath concentrations of nPB and

isopropyl bromide (iPB), and urinary metabolite concentrations of bromide and propyl

mercapturic acid were measured.

n-Propyl bromide has been marketed to replace ozone depleting solvents 1,1,I-trichloroethane

and freons®, as well as suspect carcinogens trichloroethylene and methylene chloride; chemicals

that were commonly used in industry. Very little data are currently available to evaluate human

exposure to nPB. However, there is concern that nPB may be a hematological, reproductive, or

neurological toxin, based on analogy to other brominated-propanes, animal toxicity studies, and

a limited number of case studies.

Full-shift exposure to nPB in air samples collected in workers' breathing zones ranged from 0.19

to 2.6 parts per million (ppm). All ofthe workers were exposed to nPB at levels below the

American Conference of Governmental Industrial Hygienist (ACGIH) Threshold Limit Value®

(10 ppm) as well as the industrial guideline of 25 ppm published by the EPA in their proposed

rulemaking to acceptnPB under the Clean Air Act. Isopropyl bromide was not detected in either

the air or breath samples. Exhaled breath concentrations of n-propyl bromide ranged from ND to

0.13 ppm and ND to 0.38 ppm, respectively, for pre-shift samples and post-shift samples.

Average urinary bromide concentrations were approximately 77% higher for workers than for

unexposed control subjects who were not employed by the company. Twenty-four hour average

propyl mercapturic acid concentrations measured in urine specimens from workers were over an

order ofmagnitude higher than that measured in control samples. Dermal absorption may have

contributed to some ofthe workers' exposure in addition to inhalation exposure. Workers with

the lowest breathing zone concentrations of nPB had urinary metabolite levels similar to those

measured in control specimens. At this time, the health significance ofthese levels ofurinary

metabolites is unclear.

Recommendations include, but are not limited to, substitution of nPB solvents with a less toxic

solvent (iffeasible), periodic exposure monitoring, use of gloves that are impermeable to nPB,

and routine medical examinations.

1
Introduction

The Industrywide Studies Branch ofthe National Institute for Occupational Safety and Health

(NIOSH) conducted a field study at Hamilton Sundstrand, an aerospace component

manufacturing plant in Rockford, Illinois on February 23-25, 2004. At this facility, n-propyl

bromide (nPB) was used as a vapor degreasing solvent to remove oils, chemicals, and dirt from

various parts and components prior to the inspection, surface treatments, painting, and assembly.

In this research study, we measured workers' breathing zone concentrations to nPB and

isopropyl bromide (iPB), an impurity, with standard air sampling methods in conjunction with

new methods for measuring exhaled breath and urinary metabolites.

Background

The toxicity of nPB, also named I-bromopropane (CAS no. 106-94-5), is not fully understood as

there is limited information in the published literature. The Environmental Protection Agency

(EPA, 1999; 2003) is evaluating nPB as an alternative to ozone-depleting solvents for vapordegreasing and liquid cleaning ofmetal, precision, and electronic components as well as for use

as a solvent in aerosol products and adhesives. n-Propyl bromide has been marketed to replace

1,1,I-trichloroethane, freons®, and suspect carcinogens trichloroethylene and methylene

chloride, chemicals that were commonly used in industry. Very little data are currently available

to evaluate human exposure to nPB. However, based on analogy to other brominated-propanes,

animal toxicity studies, and a limited number of case studies, there is concern that nPB may be a

hematological (blood), reproductive, or neurological toxin. (Refer to Attachment I for more

detailed information regarding the toxicity of nPB and iPB.)

Based on the uncertainty regarding the toxicity of nPB, the Occupational Safety and Health

Administration (OSHA) and NIOSH requested the National Toxicology Program (NTP) to

evaluate the toxicity ofthis chemical (OSHA, 1999; NTP, 2004). The absence ofnPB exposure

assessment information has prompted this occupational exposure study to evaluate industrial

exposures to nPB by measuring workers' personal breathing zone, exhaled breath, and urinary

metabolite concentrations.

Process Description

Hamilton Sundstrand is a subsidiary ofUnited Technologies, a diversified multi-industry

corporation which manufactures aviation engines; power fuel cells; elevators and escalators;

climate control, fire and security systems; and components for industrial and aerospace

applications. The company that participated in this study is one ofthe largest global suppliers of

advanced aerospace systems for commercial, regional, corporate, and military aircraft as well as

for sea and spacecraft. This company has 10 manufacturing sites in the U.S. and additional

facilities in Puerto Rico, Southeast Asia, and throughout Europe. Electric and flight control

systems were the primary products manufactured at the Rockford site including, but not limited

to, power generation, distribution, and control systems; constant speed drives; auxiliary

generators; electric power conversion equipment; flight control actuation and electro-magnetic

systems.

2
At this site, the main campus consists ofthree major manufacturing plants, with another

industrial plant approximately two miles away. Twenty-five hundred employees work at these

facilities; seven hundred workers are represented by the United Automobile Workers, UAW

local 592.

A nPB-based solvent (Leksol, Amity International, Inc.) is used as a vapor degreasing agent in

six departments to remove oils, chemicals, and dirt from casings, drive components, and other

parts necessary for inspection, surface treatments, painting, and assembly tasks. Eight vapor

degreasers of different makes, models, and capacities are available; however, three ofthe units

are seldom used, only a few times per month. The production schedule for this company is

dictated by customer orders, typically in small quantities ofless than 10-20 units. As such, vapor

degreasers are not continuously operated, rather parts are cleaned in batches on an "as-needed"

basis. Although approximately 100 employees have access to the degreasers, only about 30

routinely clean parts.

Vapor degreasers utilize a refrigerated cooling coil around the top ofthe interior ofthe vapor

chamber, which condenses nPB vapor into liquid droplets on the cool surface of parts to remove

surface contamination. Excess solvent drips back into the solvent sump and is recycled as the

parts slowly ascend from the vapor to condensing zones. A secondary function ofthe cooling

coil is to control solvent vapor emissions by "capping" the heated vapor zone with a refrigerated

air space, typically six to twelve inches in height. Some ofthe nPB degreasers also had a

chamber cover that was closed when the degreaser was not in use, and mechanical hoists to

remove the part racks at a programmed speed to minimize excessive vapor from being carried

out ofthe unit.

Most ofthe parts cleaning occurred in plant 6 on the main campus for Assembly Prep (one

worker was the principal user ofthe degreaser); Repair-Overhaul (two workers); Electric

Systems - Paint & Wire departments (two shifts, six workers per shift), and at plant 1 for MXM

cell/corrosion treatment and non-destructive testing (three shifts, six or seven per shift); and

Engine Control Systems - Paint & Wire departments (two shifts, six workers per shift).

In the Assembly Prep area, parts needed for the main assembly floor are cleaned in a small

(15" x 46") open-topped Delta Sonics vapor degreaser which was equipped with ultrasound

vibration to aid with cleaning, and a back plenum-slot exhaust ventilation system for additional

contaminant control. In the Repair-Overhaul room, an open-topped, medium size (~2.5' x 4')

degreaser (Branson B3550R) was used for non-destructive testing which included fluorescent

dye penetrant inspections. A chamber lid and local exhaust ducting was provided above the

condensing zone to assist with vapor emission control.

Final assembly of components were conducted in the Paint & Wire locations for both the Electric

Systems and Engine Control Systems departments. Assemblers' job tasks included degreasing,

painting, and fastening wires and identification plates prior to shipment. Spray painting was

performed with methyl ethyl ketone (MEK) and other organic solvent based paints in large

ventilated spray booths; acetone, Stoddard solvent, and isopropyl alcohol were also present in

3
these locations for clean-up activities. The Paint & Wire vapor degreasers were large semienclosed units because ofthe size ofsome components. Components were loaded into baskets

(-2.5 x 4') or crates and placed into an open framed rack. The rack was mechanically hoisted up

and over the external wall ofthe degreaseI', lowered into the vapor zone, and similarly removed

at programmed rate for effective cleaning and to reduce solvent carry-out.

A similar vapor degreasing unit was present in the MXM Cell area, Plant 1 to service anticorrosion surface treatment and non-destructive test procedures. Surface treatments were applied

by immersing parts into a series of chemical solutions and water rinses with an overhead hoist.

Phosphate coating was the principal anti-corrosion tr.eatment;chemical solutions included Turco

alkaline rust remover, sodium hydroxide, sodium fluoride, and phosphate fluoride. A number of

non-destructive test procedures were employed in the MXM Cell room to evaluate the integrity

ofmetal casings and housings: magnaflux (magnetic particles in Stoddard solvent); zyglo

(fluorescent penetrant dye); metalnox with ultrasound; and X-ray radiation. The vapor degreaser

used in MXM Cell was very similar in size and design to those installed in the Paint & Wire

locations. Even though the degreaser was enclosed, the large size and shape ofsome casings

caused solvent to pool in the parts and subsequently carried-out ofthe vapor control zone. As a

response to this problem, an auxiliary push-pull slotted local exhaust ventilation system was

installed on the sides ofthe exit conveyor to reduce workers' exposures to nPB vapors. The slot

opening in the suction plenum was approximately 4" x 5'.

Personal protective equipment used by employees included nitrile, neoprene, or butyl rubber

gloves, safety glasses, and safety shoes. Organic vapor half-face piece respirators were available

for protection against high nPBexposures such as draining spent solvent from the degreaser

sump and replenishing it with Leksol. Chemical aprons, and face shields were also required

when using the degreaser in MXM cell room. Hearing protection was also available as specified

by the Health & Safety department.

Evaluation Criteria

At present, occupational exposure limits (OELs) for nPB are not available from either OSHA

(2006) or NIOSH (1992), and suggested manufacturers' guidelines are inconsistent, ranging

from 10 to 100 parts per million (ppm) (Great Lakes Chemicals, 2005; Enviro-Tech

International, 2005). The EPA initially reviewed industry-sponsored animal studies and

suggested that 50 to 100 ppm should provide adequate protection, but cautioned that this was a

preliminary decision since it was based on limited data with considerable uncertainty (EPA,

2000). This proposal was largely based on hepatic toxicity observed in rats, not on reproductive,

hematopoietic, or neurologic effects. After reviewing industry studies (Clintrials

Biorecherchesl997a, 1997b; WIL Research Laboratories, 2000) and published literature,

Rozman and Doull (2002) concluded that neurotoxicity is the most sensitive end point and an

OEL for nPB in the range of 60 to 90 ppm should provide an adequate margin ofsafety.

On June 03, 2003, the EPA published a proposed rulemaking to accept nPB as a replacement

solvent for ozone depleting substances for general metals, precision, and electronics cleaning,

aerosol products, and adhesives (EPA, 2003). In this proposed rule, the EPA recommends an

4
industrial exposure guideline for nPB of25 ppm over an 8-hr work shift. The proposed

rulemaking is currently being re-assessed by the EPA. Albemarle Co. (2003), one ofthe

domestic suppliers ofnPB solvents, also recommends an exposure guideline for nPB equal to 25

ppm as an 8-hour time weighted average (TWA) concentration. In 2005, ACGIH published a

recommended Threshold Limit Value® (TLV) for nPB as a 10 ppm, 8-hr TWA based on

suspected neurological toxicity (ACGIH, 2006). As one can see from these exposure guidelines,

the OELs for nPB recommended by different organizations vary by an order ofmagnitude.

Following a case study ofreproductive and hematological health effects in workers exposed to

iPB in an electronics plant (Kim et aI., 1996; Park et aI., 1997), the Republic ofSouth Korea

promulgated an OEL for iPB of 1 ppm, measured as an8-hour TWA. No other OELs are

presently published for iPB. Occupational exposure criteria for two ofthe urinary metabolites of

nPB which were analyzed at these facilities (e.g., bromide and propyl mercapturic acid) are

currently unavailable.

Methods

In this research study, we measured nPB inhalation exposures with standard air sampling

methods in conjunction with new methods for measuring exhaled breath and urinary metabolites.

Employees voluntarily participating in the study were informed ofthe study requirements and

provided their written consent in accordance with Human Subjects Review Board protocol. A

total of 11 workers were included, each ofwhom worked with or was expected to be in the

vicinity of vapor degreasers using nPB. The workers also wore a light-weight air sampling

device on 2 consecutive days, provided pre- and post-shift exhaled breath samples, and all of

their urine specimens over a 48-hour period. The air and breath samples were analyzed for nPB

as well as iPB, a low level contaminant in nPB solvents. The urine samples were analyzed for

bromide (Br) ion and propyl mercapturic acid (PMA), also called N-acetyl-S-(n-propyl)-Lcysteine.

Personal breathing zone exposures and exhaled breath samples were collected with Anasorb

carbon molecular sieve (CMS) sorbent tubes. The sorbent tubes were desorbed with 1 milliliter

(ml) of carbon disulfide, and analyzed for nPB and iPB by gas chromatography with flame

ionization detection (GC-FID) via NIOSH method 1025 (NIOSH, 2003a). The limit of detection

(LOD) for this method is 1 ~g which equates to a minimum detectable concentration (MDC) of

0.017 ppm in air using the maximum recommended air sampling volume of 12 liters and a MDC

of 0.066 ppm in an exhaled breath volume of 3 liters. Qualitative evaluation ofskin contact

potential was conducted by visual observation ofjob tasks since effective quantitative skin

exposure measurement methods do not exist for compounds, such as nPB, that are volatile and

readily penetrate intact skin.

To obtain data on nPB metabolites excreted by humans, all ofthe workers' urine voids over a

48-hour period were collected, including the amount excreted while away from work. The

specimens were collected as composite samples over sequential time intervals: 1) at work,

2) after work but before bedtime, and 3) upon awakening. Each sampling survey was intended to

occur over a 48-hour period that started at the beginning ofthe work week (Monday, pre-shift),

5
following a weekend ofno exposure and end before the work shift on Wednesday. [However,

three (out offour) employees in plant 6, and one (out ofseven) employees in plant 1 worked

with nPB over the weekend.] For comparison, single "spot" control samples were collected from

twenty-one unexposed office workers who were not employed by this company.

Urine specimens were collected in nitric acid rinsed Nalgene® bottles [high density polyethylene

(llDPE)] and immediately chilled in 10 quart coolers with gel ice that were individually.supplied

to each participant. Upon the end ofthe collection period, three-25 ml sample aliquots were

dispensed into nitric acid rinsed HOPE bottles and immediately frozen on carbonic .acid (dryice). The total urine volume for this collection period was also measured with a graduated

cyclinder. In addition to Br and PMA, the specimens were also analyzed for creatinine (cr).

Bromine

Bromine (Br) was measured with.inductively coupled plasma/mass spectrometry (ICP/MS;

Varion Ultra-mass 700) using yttrium as an internal standard (Allain et aI., 1990; Ichihara et aI.,

2004; Kawai et aI., 2001). The LOD for bromine was 90 micrograms per liter (Jlg/I). One ml of

each sample was diluted to 10 ml with 1% nitric acid prior to analysis. Analytical.standards and

quality control samples were prepared using Uri-sub, a synthetic urine solution. This was

necessary because background concentrations of bromine may be present in pooled urine from

the general population.

Propyl mercapturic acid

The urine specimens were analyzed for PMA, one ofthe major mercapturic acid metabolites of

nPB (Grenby and Young, 1960; Jones and Walsh, 1979). Fourml aliquots ofthe urine

specimens were loaded onto a solid phase extraction cartridge, rinsed with three ml ofa

methanol-acidified water mixture (pH = 3); PMA was then extracted in four ml of acetone, dried

under nitrogen, and reconstituted in one ml ofmethanol. Analysis was performed using high

performance liquid chromatography (HPLC) with electrospray ionization-tandem mass

spectrometry (ESI-MS/MS) for improved sensitivity and specificity (e.g., confirmation of

chemical identity).

Creatinine

Creatinine was analyzed using Sigma diagnostics test kit, procedure #555. Room temperature

urine specimens were diluted by a factor of 20 (or 40 ifvery concentrated) and mixed with six ml

of alkaline picrate. After 10-15 minutes, color analysis ofthe creatinine-picrate complex was

performed with a spectrophotometer (Milton Roy Spectronic 20 D). A 0.2 ml aliquot of acid

reagent was then added and the specimen was re-analyzed after five minutes; positive results

from the second analysis were subtracted from the first measurements as it is due to interfering

compounds.

Creatinine is a protein by-product excreted in urine due to the metabolism ofcreatine from

muscle exertion. It is often used to adjust urine data due to different levels ofphysical activity,

6
hydration, and urine concentrations between different individuals. The urine data in this report,

however,are only presented as unadjusted concentrations, either mg/l or p.g/l for Br and PMA,

respectively. Once the data are compiled from multiple sites in this study, the urine data will be

adjusted ("normalized") for creatinine (mg Br/gm creatinine or p.g PMA/gm creatinine) for

publication in scientific journals.

Results

Table lA presents the air sampling results collected in workers' breathing zones over two full

work shifts. Table 1B and 1C provide the data stratified separately for each plant. The TWA

concentrations for all jobs in both plants ranged from 0.19 to 2.6 ppm with daily averages of 0.99

and 1.2 ppm. All workers' TWA exposures were less than 10 ppm. Iso-propyl bromide was not

detected in any ofthe air samples. The two highest TWAs occurred in MXM cell department on

a day when the degreaser was used thirteen times. Although the highest exposures occurred in

MXM cell (plant 1) when conducting non-destructive testing, the average TWA exposure in

plant 6 was greater than for plant 1 on both days (1.5 versus 0.69 and 1.5 versus 1.09,

respectively for day 1 and day 2). One reason may be that three ofthe Assemblers who were

monitored in plant 1,collectively used the degreaser once and only walked near theses areas on a

few occasions. Workers in plant 6 reported infrequent use ofthe degreasers because they

worked over the weekend.

Tables 2A, 2B, and 2C provide a summary ofthe breath concentrations for nPB, respectively for

both plants combined, plant 1, and plant 6. The nPB concentrations measured in the post-shift

samples ranged from non-detectable to 0.38 ppm. Ten (out of22) samples had detectable levels

ofnPB in the pre-shift samples, ranging from ND to 0.13 ppm. Isopropyl bromide was not

detected in any ofthe breath samples. The average breath concentrations measured in each

building were nearly identical. However, nPB was detected in low concentrations (0.022-0.11

ppm) from air samples collected in the nurse's office during breath collection periods in Plant 1

but not Plant 6. This may have caused sample contamination.

The average Br concentration from urine samples collected before the work-week began was 8.8

milligrams per liter (mg/l) for both plants combined (Table 3A). For comparison, the average Br

concentration was 4.0 mg/l in spot samples from control subjects who were not employed by this

company. Moreover, the 24-hour.average concentrations of urinary Br for all workers were

approximately 77% greater than the control subjects. In plant 1, the average 24-hour Br

concentrations were similar to the control average, but were two to three times higher in plant 6.

The data for PMA are provided in Table 4A, 4B, and 4C, which show a similar trend as the

average before work week concentrations for workers was approximately 44% higher than the

average calculated from control specimens. Furthermore, the average 24-hour concentrations of

PMA from all workers were .an order ofmagnitude higher than controls for both work days. The

most heavily exposed workers in plant 6 had the highest PMA in urine concentrations, however,

the average 24-hour PMA levels in plant 1 were also at least four times as high as controls.

The potential for solvent splashing and dermal contact exists with vapor degreasing processes,

especially in MXM cell department because ofthe shape ofthe parts. The gloves observed to be

7
used in these departments (nitrile and neoprene) do not provide adequate protection for more

than a few hours.

Statistical analyses were not conducted for the data collected at this site since only 11 workers

participated in the monitoring. Statistical analyses will be performed after all ofthe data

collected at separate sites are pooled into larger data bases.

Conclusions

• All ofthe workers' full-shift exposures were below the industrial guideline of25 ppm

proposed by the EPA as well as the ACGIH TLV® of 10 ppm.

• The condensing coils and exhaust ventilation provided for the vapor degreasers is

relatively effective in controlling nPB air emissions from these operations in both plants,

given the observed production rates.

• Workers' exposures to iPB were not detected with a minimal detected concentration

(MDC) well below 1 ppm, the only occupational exposure limit available (published by

South Korea).

• The post-shift breath monitoring showed measureable levels ofnPB but not iPB.

• With the exception of one sample, breath concentrations ofnPB were not detected in preweek samples.

Dermal contact with recently degreased parts may contribute to the workers' exposures.

nPB is appreciably absorbed through workers' intact skin, which contributes to their

overall absorbed dose.

Average 24-hour concentrations ofthe urinary Br were 77% higher for workers than for

control subjects.

Average 24-hour concentrations ofthe urinary PMA measured in worker specimens were

at least 10 times as high as PMA concentrations measured in control specimens.

The conclusions drawn are based on the data from the grouped population ofworkers.

These data demonstrate that workers using degreasersare exposed to and are excreting

nPB metaboles. However, the health significance of an individual's urine metabolite

level is uncertain.

Recommendations

Human health effects from exposure to nPB are not fully understood as there are only a few

reports in the published literature. The occupational exposure criteria of25 ppm suggested by

the EPA and some solvent manufacturers are largely based on limited data observed in animal

8
toxicity studies. As additional scientific information becomes available, the OEL currently

proposed may, in fact, be lowered. Therefore, NIOSH scientists believe it is prudent to reduce

occupational exposure ofnPB to the lowest feasible levels.

To reduce the risk ofhazardous exposures in the work environment, industrial hygiene principles

incorporate the following hierarchy of exposure control, in decreasing order ofpnbference (and

effectiveness):

i) Eliminate a toxic substance by substituting it with a less toxic one or by process

changes,

ii) Install engineering controls to remove or reduce the airborne contaminants, preferably

at the point of emission using: local exhaust ventilation; isolation of contaminant

emissions away from worker positions; or by process changes,

iii) Use of administrative controls to reduce individual exposures by altering or rotating

job tasks and work schedules, thereby reducing high exposure durations, and

iv) Use ofpersonal protective equipment (PPE), such as respiratory protection, gloves,

aprons, etc., to reduce the absorbed dose from potential exposure. Although PPE is

frequently used because it is a cheaper and easier method of control, it is the least

desirable because it is not always effective. NIOSH policy is that PPE should only be

used when engineering controls are infeasible; during the interim period when

engineering controls are being installed or repaired; or when engineering controls are

not effective in reducing exposure below hazardous levels.

More specific recommendations to minimize workers' exposures to nPB at this facility are

provided below:

1. Eliminate nPB based solvents iffeasible by using a less toxic substitute. It is

advisable to consult with technical experts and solvent distributors to evaluate if

there are any suitable alternative solvents that are less toxic which perform in

accordance with engineering specifications.

2. Employee exposures to nPB should be periodically re-evaluated. Ifmonitoring

results exceed relevant criteria, install engineering controls consisting oflocal

exhaust for the degreaser and provide make-up air ventilations systems to reduce

airborne nPB concentrations. Design specifications are available in the ACGrn

Industrial Ventilation Manual, 25th edition (2006). In addition, a routine

maintenance schedule must be implemented to ensure effective performance of

the equipment.

3. Respiratory protection should be provided for those workers who desire to use it

when operating the vapor degreaser or ifthe controls are not effective in reducing

exposures sufficiently. Only NIOSH approved air purifying respirators with

organic vapor cartridges or NIOSH approved air supplied respirators should be

used. The use ofrespiratory protection requires the implementation of a

comprehensive respiratory protection program in accordance with OSHA

regulations (29 CFR 1910.134) and NIOSH recommended procedures (NIOSH,

9
1987). A minimal acceptable program must be managed by a competent person

and include: written procedures; proper selection; user training; routine cleaning

and inspection; proper storage; surveillance ofwork conditions and worker

exposures; program audits; medical determination of user fitness; and use of

approved respirators.

4. n-Propyl bromide readily penetrates intact skin and common glove materials. The

relatively low TWA air concentrations coupled with high PMA metabolites

suggests that dermal contact and absorption of nPB is substantial for some

workers using the vapor degreasers. When skin contact potential with nPB or

parts recently removed from the degreaser is high, appropriate gloves, arm

sleeves, aprons or other PPE should be used as appropriate. Solvent

manufacturers recommend use ofmultiple layer laminates for protection against

nPB. These include, but are not limited to, VitonTM, 4H (pE/EVAL)TM, and

Silver ShieldTM. Other more common glovelPPE materials (e.g., latex, nitrile,

neoprene, butyl rubber, PVC, etc.) do not adequately preventnPB from

penetrating the PPE material for more than 30 minutes to a few hours. This may

include time after the glove is contaminated even though it is no longer worn by a

worker. The more common gloves may still be required for protection against

other chemicals used in these areas. Hence, it is advisable to consult with

technical experts and safety supply vendors to select an array of gloves needed in

these departments. Periodic training of employees is important to prevent them

from using the wrong gloves for different applications.

5. If alternative solvents are not feasible, use nPB solvents that have the lowest iPB

contamination as is possible. Based on the non-detectable iPB results, it appears

that nPB solvents used at your facilities do not contain excessive iPB

contamination. The ASTM (2001) standard for iPB contamination in nPB

solvents is 0.10%. In the EPA proposed rulemaking (2003) to accept nPB

solvents, a use restriction includes using nPB solvents with an iPB contamination

not exceeding 0.05%, before blending into products. It is advisable to confirm

that the nPB solvents at your sites meet this criterion.

6. Company management must maintain an awareness ofthe latest scientific

information regarding occupational exposure guidelines for nPB as well as

relevant health, safety, and environmental standards from regulatory agencies.

7. Employees potentially exposed to nPB should be provided with routine medical

examinations. Reports of health effects should be referred to a health care

provider who specializes in occupational or environmental medicine.

10
Table lAo

Summary ofworkers' TWA8air sample concentrations of n-propyl bromide

and isopropyl bromide for plants I and 6 combined.

Hamilton Sundstrand

Rockford, IL

National Institute for Occupational Safety and Health

Centers for Disease Control and Prevention

IWSB232.12

TWA Air Concentration (ppml

Chemical Measure (n = 11)

Day I Day 2

Average 0.99 1.2

nPBc

Range 0.19 - 2.1 0.11-2.6

Average - -

iPBd

Range NDe ND

Table lB.

Summary ofworkers' TWA8 airsample concentrations of n-propyl bromide

and isopropyl bromide for plant 1.

TWA Air Concentration (ppml

Chemical Measure (n= 7)

Day 1 Day 2

Average 0.69 1.1

nPBc

Range 0.19 -1.1 0.11- 2.6

iPBd

Average - -

Range NDe ND

11
Table IC.

Summary ofworkers' TWAa air sample concentrations of n-propyl bromide

and isopropyl bromide for plant 6.

Hamilton Sundstrand

Rockford, IL

National Institute for Occupational Safety and Health

Centers for Disease Control and Prevention

IWSB232.12

TWA Air Concentration (ppmr

Chemical Measure (n == 4)

Day 1 Day 2

Average 1.5 1.5

nPBc

Range 0.82 - 2.1 1.3 -1.6

Average - - iPBd

Range NDe ND

Footnotes for Tables lA, IB, and Ie:

a) TWA = time weighted average. It is used when multiple samples are collected OVer the work shift

to calculate the average exposure concentration "pro-rated" for time.

Example:

TWA = [(time 1 x cone. 1) + (time 2 x cone. 2)... + (timei x cone.i)] + total time for both sample 1 and 2

plus all additional samples (i)

b) Units are in parts per million by volume; the amount of bromopropane per 1 million parts of air.

c) nPB= n-propyl bromide (also called I-bromopropane).

d) iPB = isopropyl bromide (also called 2-bromopropane).

e) ND = non-detectable.

12
Table2A.

Summary ofworkers' breath concentrations of n-propyl bromidea for plants 1 and 6 combined.

Hamilton Sundstrand

Rockford, IL

National Institute for Occupational Safety and Health

Centers for Disease Control and Prevention

IWSB232.12

nPB Breath concentration (ppmt

Date Measure (n=l1)

Pre-shift Post-Shift

Average - 0.23

Day 1

Range NDe 0.11- 0.38

AverageC 0.11 (n = 5)d 0.17 (n = 8t

Day 2

Range ND-O.B NO-0.21

Average 0.097 (n =st n.a. e

Day 3

Range ND-O.B n.a.

Table2B.

Summary ofworkers' breath concentrations of n-propyl bromidef for plant 1.

nPB Breath concentration (ppm)g

Date Measure (n =7)

Pre-shift Post-Shift

Average - 0.23

Day 1

Range NOn 0.12 - 0.38

Averageh 0.11 (n =4) 0.16 (n =4)

Day 2

Range NO - 0.13 ND~0.19

Average 0.096 (n =2) 1

n.a.

Day 3

Range NO-0.13 n.a.

13
Table 2e.

Summary ofworkers' breath concentrations of n-propyl bromide8 for plant 6.

Hamilton Sundstrand

Rockford, IL

National Institute for Occupational Safety and Health

Centers for Disease Control and Prevention

IWSB232.12

nPB Breath concentration (ppml

Date Measure (n=4)

Pre-shift Post-Shift

Average - 0.23

Day 1

Range NDc 0.11- 0.33

Average I 0.18 - Day 2

Range ND-0.12 0.13-0.21

AverageC0.098 (n = 3)° e n.a.

Day 3

Range ND-0.12 n.a.

Footnotes for Tables 2A, 2B, and 2C:

a) iPB was not detected in any ofthe breath samples.

b) Units are in parts per million by volume; the amount of bromopropane in 1 million parts of breath.

c) ND = non-detectable. Only detectable values were used to calculate averages.

d) n varies because only detectable values, in lieu of zero or imputed values, were used to calculate averages.

e) Not applicable. Only a "before work" breath sample (e.g. 16-hour post shift) was collected on day 3.

f) Average wasn't calculated because nPB was detected in only one breath sample from this collection period.

14
Table3A.

Summary ofworkers' bromine eoneentrations in urine for plants 1 and 6 eombined.

Hamilton Sundstrand

Rockford, IL

National Institute for Occupational Safety and Health

Centers for Disease Control and Prevention

IWSB232.12

Chemieal Job Day 1, Before Work8

Ran2e Avera2e

Plants 1& 6 1.8 -22 8.8

Bromine (n = 11)

(mg/liter)b

ControlsC0.98 - 16 4.0

Chemical Job Day 1, 24-Hr.Coneentrationd Day 2, 24-Hr. Concentration

Ran2e Averae;e Ran2e Avera2e

Bromine Plants 1& 6 1.9 - 21 7.7 2.8 -15 6.5

(mglliter) (n = II)

Table 3B.

Summary ofworkers' bromine concentrations in urine for plant 1.

Chemical Job Day 1, Before Work8

Rane;e Averae;e

Plant I 1.8 -13 4.8

Bromine (n = 7)

(mg/liter)b

ControlsC0.98 - 16 4.0

Chemical Job Day 1, 24-Hr. Coneentrationd Day 2, 24-Hr. Concentration

Rane;e Avera2e Rane;e Avera2e

Bromine Plant 1 1.9 - 8.1 4.1 2.8-8.2 4.6

(mg/liter) (n= 7)

15
Table3C.

Summary ofworkers' bromiue concentrations in urine for plant 6.

Hamilton Sundstrand

Rockford, IL

National Institute for Occupational Safety and Health

Centers for Disease Control and Prevention

IWSB232.12

Chemical Job Day 1, Before Worka

Ran2e Avera2e

Plant 6 8.7-22 16

Bromine (n :=: 4)

(mglliterl

ControlsC0.98 -16 4.0

Chemical Job Day 1, 24-Hr. Concentrationd Day 2, 24-Hr. Concentration

Rane:e Averae:e Ran2e Averae:e

Bromine Plant 6 7.6 ~21 14 4.2 -15 9.7

(mglliter) (n = 4)

Footnotes for Tables 3A, 3B, and 3C:

a) Sample was collected before or near the start ofthe work shift, after the weekend away from work.

b) Units are in milligrams ofbromine per liter of urine.

c) Control samples were collected from 2loffice workers unexposed to nPB, not employed by this company.

d) 24-Hour concentrations were calculated from 3 combined samples of all urine specimens collected at work;

after work before bedtime; and upon waking.

16
Table 4A.

Summary ofworkers' propyl mercapturic acid concentrations in urine for plants 1 and 6

combined.

Hamilton Sundstrand

Rockford, IL

National Institute for Occupational Safety and Health

Centers for Disease Control and Prevention

IWSB 232.12

Chemical Job Day 1, Before Work

Ran2e Avera2e

Plants 1 & 6 ND~499 85.9

PMN (n = 11)

(/lglliter)b

ControlsC NDd~207 59.7

Chemical Job Day 1, 24-Hr. Concentratione Day 2, 24-Hr. Concentration

Ran2e Avera2e Ran2e Avera2e

PMA Plants 1 & 6 15.6 ~2390 649 4.99 2510 571

(~~/liter) (n = 11)

Table 4B.

Summary ofworkers' propyl mercapturic acid concentrations in urine for plant 1.

Chemical Job Day 1, Before Work

Ran2e Avera2e

Plant 1 ND-23.4 10.8

PMN (n = 7)

(/lglliter)b

ControlsC NDd~207 59.7

Chemical Job Day 1, 24-Hr. Concentratione Day 2, 24-Hr. Concentration

Ran2e Avera2e Ran2e Avera2e

PMA Plant 1 15.6 - 883 250 4.99 -755 268

(~~/liter) (n= 7)

17
Table 4C.

Summary ofworkers' propyl mercapturic acid concentrations in urine for plant 6.

Hamilton Sundstrand

Rockford, IL

National Institute for Occupational Safety and Health

Centers for Disease Control and Prevention

IWSB 232.12

Chemical Job Dav 1, Before Work

Range Average

Plant 6 52.6 - 499 217

PMAa (n :=: 4)

(/lglliter)b

NDd Controls -207 C

59.7

Chemical Job Day 1, 24-Hr. Concentratione Day 2, 24-Hr. Concentration

Range Average Range Average

PMA Plant 6

(/lglliter) (n = 4) 607 - 2390 1350 427-2510 1100

Footnotes for Tables 4A, 4B, and 4C:

a) PMA = propyl mercapturic acid.

b) Units are in micrograms ofpropyl mercapturic acid per liter of urine. (One microgram is one thousand

times lessthan a milligram.)

c) Control samples were collected from 21office workers unexposed to nPB, not employed by this company.

d) ND = non-detectable.

e) 24-Hour concentrations were calculated from 3 combined samples of all urine specimens collected at work;

after work before bedtime; and upon waking.

18
Attachment I

Toxicity of n-propyl bromide and isopropyl bromide

The molecular structure of bromopropanes is a simple three carbon alkane chain containing a

single bromine substitution. There are two bromopropane isomers: n-propyl bromide [(nPB)

also called 1-bromopropane; CAS No. 106-94-5] and isopropyl bromide [(iPB) also called 2-

bromopropane; CAS No.75-26-3]. Prior to the lastseveral years, nPB was primarily used to

manufacture pharmaceuticals, pesticides, and other chemicals typically in well controlled closed

processes. An international agreement between a number ofindustrial nations restricts the

manufacture and use of ozone depleting substances including some compounds which were

widely used throughout general industry: 1,1 ,I-trichloroethane and chlorofluorocarbons

(freons®). In an effort to develop alternatives to replace these ozone depleting solvents, nPB

products have been marketed, or are being considered, for metal cleaning/degreasing, automotive

degreasing, electronics cleaning, precision cleaning (e.g., plastics, optics, and medical

equipment), aerosol products, adhesive solvents, paint and coating solvents, textile dry cleaning,

printing inks, and asphalt blending (EPA, 2003; Dead Sea Bromine, 1999; Petroferm, 2000).

Products containing potential carcinogens trichloroethylene and methylene chloride are also

candidates for alternative solvents, especially since the OSHA methylene chloride standard

imposes more stringent occupational exposure and medical surveillance criteria with increased

compliance costs. Currently, the principal application for nPB, in terms of quantities used, is for

a vapor degreasing and liquid cleaning agent as well as spray adhesive solvent (EPA, 2003).

However, the need to find suitable alternative solvents could expand nPB market applications,

substantially increasing the quantities manufactured.

The first reports ofhealth effects for bromopropanes occurred in 1996 in a Korean electronics

plant where iPB was used as a cleaning solvent for electronic switches (Kimet aI., 1996; Park et

aI., 1997). An epidemiology case study of 33 workers revealed that approximately two-thirds

were experiencing reproductive disorders affecting both genders (e.g., low sperm concentrations,

low motility or deformed sperm in men; and amenorrhea and elevated follicle stimulating

hormone in women) (Kim et aI., 1996). Further, seven workers had pancytopenia (e.g., reduced

blood cell counts). An exposure-health effect association was obscured in this study since

breathing zone monitoring was not performed, and the significance ofreported dermal contact

and briefshort-term exposure to very high air concentrations is unclear. Ichihara et ai. (1997;

1999) conducted a similar study at a chemical plant manufacturing iPB in China. Although

severe reproductive disorders were not observed, reduced sperm concentrations and motility as

well as decreased hemoglobin and hematocrit were suspected by the authors to be related to iPB

exposure.

Subsequent to these occupational investigations, a series ofrat studies were conducted in Japan

with iPB to evaluate male reproductive and female reproductive or hematopoietic toxicity. In a

review ofthe literature, Takeuchi et ai. (1997) concluded that iPB impairs: (i) the testes,

especially spermatogonia, (ii) ovarian function by disturbing the estrous cycle, damaging

primordial follicles and oocytes, (iii) bone marrow causing pancytopenia. Neurologic effects in

rats exposed to iPB were also discovered by Yu et ai. (1999; 2001).

19
There has been incentive to use nPB in lieu ofiPB because ofthe perception that nPB has lower

toxicity. There are several reports in the published literature regarding epidemiological and

toxicological studies of nPB which are contrary to this supposition. In a 2001 report, Yu .et aI.

(2001) demonstrated peripheral and possibly central neurotoxicity in rats but did not show

reproductive or hematologic .effects. Several additional reports have concluded that nPB

produces dose dependant estrous cycle irregularities (Yamada et aI., 2003; Takeuchi et aI.,

2001); spermiation destruction (Takeuchi et ai., 2001; Ichihara et aI., 2000a); reproductive and

developmental toxicity (NTP, 2002; 2004; Ichihara et aI., 2005); increased liver enzymes (Lee et

aI., 2005); and peripheral and central neurotoxicity (Yu et aI., 2001; Ichihara et aI., 2000b) in rats

at similar dose levels that produced these effects by iPB. Ichihara et aI. (2000b) concluded that

nPB appeared to be a more potent neurotoxin than iPB. This conclusion is supported by several

rat studies which have shown ataxic gait and hyper-excitability ofthe central nervous system,

particularly at higher doses (Fueta et aI., 2000, 2002a, 2002b, 2004; Honma et aI., 2003; Wang et

aI.,2003).

Garner et aI. (2006) published a metabolism study which investigated the disposition and

excretion of nPB following intravenous, inhalation and dermal administration using mice and

rats of both genders, metabolic inhibitors, and genetically altered animals. The authors

concluded that metabolism and excretion were independent ofroute of administration.

Elimination of nPB was very rapid with a half life under one hour, mostly via exhalation.

Urinary excretion occurred by two principal mechanisms: dehalogenation by cytochrome P-450

and conjugation with glutathione. Minor metabolites were also observed indicating several other

pathways for elimination.

Two case studies in the US have been published which describe decreased peripheral nerve

functioning for three foam cushion workers using spray adhesives containing over 50% nPB

(lchihara, et aI. 2002) and a worker who performed metal stripping using a degreasing solvent

with approximately 95% nPB (Sclar, 1999). Presenting symptoms included numbness, weakness

oflower extremities, staggering, and parasthesia or dysesthesia. The authors concluded that nPB

likely caused the peripheral and central nervous system defects in these workers.

NIOSH has conducted Health Hazard Evaluations (HHEs) at two foam cushion fabricators and

an aircraft seat cushion manufacturer where nPB was used as a spray adhesive solvent (NIOSH,

2003b; 2002a; 2002b). Full-shift nPB exposures at these plants identified numerous excursions

exceeding 100 ppm, one recommended exposure guideline by some solvent distributers. For

comparison, the 2003 proposed EPA industrial exposure guideline is 25 ppm, and the ACGIH

TLV® published in 2005 is 10 ppm, measured as an eight-hour time-weighted average (TWA).

At the aircraft seat cushion plant, full-shift nPB exposures ranged from 60 to 381 ppm, and 67 of

69 measurements exceeded 100 ppm (NIOSH, 2002a). Analysis of complete blood counts

obtained from 43 (61%) ofthe aircraft cushion workers did not establish nor exonerate

abnormalities associated with nPB exposure. A reproductive health questionnaire was also

administered but the results were also inconclusive.

20
Toraason et al. (2006) conducted genotoxic studies to assess DNA damage, in vitro, and from 64

workers employed at two ofthe above HHE foam fabricating plants NIOSH investigated using

PB-based adhesives. The authors concluded that limited evidence existed at these facilities to

show exposure to nPB was associated with increased DNA damage.

21
References

ACGIH [2006]. 2006 TLVs® and BEIs®: Threshold limit values for chemical substances and physical

agents. Cincinnati, OH: American Conference ofGovernmental Industrial Hygienists.

ACGIH [2006]. Industrial Ventilation Manual, 25th edition. Cincinnati, OH: American Conference of

Governmental Industrial Hygienists.

ASTM [2001]. D6368-00 Standard specification for vapor-degreasing grade and general grade normalpropyl bromide. West Conshohocken, PA: American Society for Testing Materials.

Albemarle Corp [2003]. Albemarle workplace exposure guideline for AbzolJ cleaners. Baton Rouge,

LA. www.albemarle.com/abzuserman.htm. accessed June X, 2003.

Allain P., Mauras Y., Douge C., Jaunault L, Delaporte T., Beaqgrand C. [1990]. Determination ofiodine

and bromine in plasma and urine by inductively coupled plasma spectrometry. Analyst 115:813-815.

Clintrials Biorecherches [1997a]. A 28-day inhalation study ofa vapor formulation ofALBTA 1 in the

albino rat. Bio-Research project no. 91189. Senneville, Quebec, Canada H9X 3R3. Sponsored by

Albermarle Corp. Available from USEPA docket A-91-42, document X-A-4.

Clintrials Biorecherches [1997b]. A 13-week inhalation study ofa vapor formulation ofALBTA 1 in the

albino rat. Bio-Research project no. 91190. Senneville, Quebec, Canada H9X 3R3. Sponsored by

Albermarle Corp. Available from USEPA docket A-91-42, document X"A-5.

Dead Sea Bromine [1999]. Applications ofn-Propyl Bromide. www.deadseabromine.com. Accessed

August 2001.

Enviro Tech International, Inc. [2005]. Material Safety Data Sheet for Ensolv®. Melrose Park, IL

www.Ensolv.com. Issue date February 17,2005.

EPA [1999]. Protection of Stratospheric Ozone: Listing ofsubstitutes for ozone depleting substances.

Request for data and advanced notice of proposed rulemaking.. 40 CFR Part 82. Federal Register:

February 18, 1999. Vol 64, No 32, pages 8043-8048.

EPA [2000]. Protection of Stratospheric Ozone: Notice 14 for significant new alternatives policy

program. 40 CFR Part 82. Federal Register: December 18, 2000. Vol 65, No 243, pages 78977-78989.

EPA [2003]. Protection of Stratospheric Ozone: Listing ofsubstitutes for ozone depleting substances. nPropyl bromide. Proposed rule. 40 CFR Part 82. Federal Register: June 3, 2003. Vol 68, No 106, pages

33284-33316.

FuetaY, Ishidao T, Kasai T, Hori, H, Arashidani K. [2000]. Decreased paired-pulse inhibition in

the dentate gyrus ofthe brain in rats exposed to 1-bromopropane vapor. .J Occup Health 42:149-

151.

Fueta Y, IshidaoT, Arashidani K, Endo Y, Hori H. 12002a]. Hyperexcitability ofthe

hippocampal CA1 and the dentate gyrus in rats subchronically exposed to a substitute for

chlorofluorocarbons, 1-bromopropane vapor. .JOccup Health 44:156-165.

22
Fueta Y, Fukunaga K, Ishidao T, Hori H [2002b]. Hyperexcitability and changes in activities

ofCa2+/calmodulin-dependent kinase II and mitogen-activated protein kinase in the

hippocampus ofrats exposed to I-bromopropane. Life Bc 2:521-529.

Fueta Y, Fukuda T, Ishidao T, Hori H [2004]. Electrophysiology and immunohistochemistry

in the hippocampal cal and the dentate gyrus ofrats chronically exposed to I-bromopropane, a

substitute for specific chlorofluorocarbons. Neuroscience 124(3):593-603.

Garner C, Sumner S, Davis J, Burgess J, Yueh Y, Demeter J, Zhan Q, Valentine J, Jeffcoat A, Burka t,

Mathews J [2006]. Metabolism and dispostionof 10bromopropane in rats and mice following inhalation

or intravenous administration. Toxicol App Pharmacol e-pub February 2006.

Great Lakes Chemicals {2005]. Material Safety Data Sheet for n-propyl bromide. West Lafayette, IN.

www.el.greatlakes.com. Issue date March 7, 2005.

Grenby TH, Young L [1960]. Biochemical studies ofn-propylmercapturic acid from n-propyl halides.

Biochem J75:28-33.

Houma, T., Suda, M., Miyagawa, M. [2003]. Inhalation of I-bromopropane causes excitation in

the central nervous system ofmale F344 rats. Neurotox 24:563-575.

Ichihara G, Yu S, Kamijima M, Ting X, Wu X, Takeuchi Y [1997]. An occupational health investigation

of a factory producing 2-bromopropane in China. J Occup Health 39 suppl:S327.

Ichihara G, Ding X, Yu X, Wu X, Kamijima M, Peng S, Jiang X, Takeuchi Y [1999]. Occupational

health survey on workers exposed to 2-bromopropane at low concentrations. Am J Ind Med 35:523-531.

Ichihara G, Yu X, Kitoh J,Asaeda N, Kumazawa T, Iwai H, Shibata E, Yamada T, Wang H, Xie Z,

Maeda K, Tsukamura H, Takeuchi Y [2000a]. Reproductive toxicity of I-bromopropane, a newly

introduced alternative to ozone layer depleting solvents, in male rats. Toxicol Sci 54:416-423.

Ichihara G, Kitoh J, Yu X, Asaeda N, Iwai H, Kumazawa T, Shibata E, Yamada T, Wang H, Xie Z,

Takeuchi Y [2000b]. I-Bromopropane, an alternative to ozone layer depleting solvents, is dosedependently neurotoxic to rats in long-term inhalation exposure. Toxicol Sci 55:116-123.

Ichihara G, Miller JK, Ziolkowska A, Itohara S, Takeuchi Y [2002]. Neurological disorders in three

workers exposed to I-bromopropane. J Occup Health 44: 1-7.

Ichihara G, Li W, Ding X, Peng S, Yu X, Shibata E, Yamad T, Wang H, Itohara S, Kanno S, Sakai K, Ito

H, Kanefusa K, and Takeuchi Y [2004]. A Survey on Exposure Level, Health Status, and Biomarkers in

Workers Exposed to I-Bromopropane. Amer J Ind Med 45:63-75.

Ichihara G [2005]. Neuro-reproductive toxicities of I-bromopropane and 2-bromopropane. Int Arch

Occup Environ Health 78:79-96.

Jones AR, Walsh DA [1979]. The oxidative metabolism of I-bromopropane in the rat. Xenobiotica

9(12):763-772.

23
Kawai T, Takeuchi A, Miyama Y, Sakamto K, Zhang ZW, Higashikawa K, Ikeda M [2001]. Biological

monitoring of occupational exposure to I-bromopropane by means of urinalysis for I-bromopropane and

bromide ion. Biomarkers 6(5):303-312.

KimY, Jung K, Hwang T, Kim H, Park J, Kim J, Park J, Park 0, Park S, Choi K, Moon Y [1996].

Hematopoietic and Reproductive Hazards ofKorean Electronic Workers Exposed to Solvents Containing

2-Bromopropane. Scan J Work Environ Health 22:387-391.

Lee SK, Jo SW, Jeon rw, Jun ill, Jin CH, Kim GH, Lee DJ, Kim T-O, Lee E-S, Jeong TC

[2005]. Hepatotoxicity ofI-bromopropane and conjugation with glutathione in male ICR mice.

Arch Pharm Res 28:1177-1182.

NIOSH [1987]. Guide to Industrial Respiratory Protection. Cincinnati, OH: U.S. Department ofHealth

and Human Services, Public Health Service, Centers for Disease Control and Prevention, National

Institute for Occupational Safety and Health, DHHS (NIOSH) Publication No. 87-116.

NIOSH [1992]. Recommendations for occupational safety and health: compendium of policy documents

and statements. Cincinnati,OH: U.S. Department of Health and Human Services, Public Health Service,

Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, DHHS

(NIOSH) Publication No. 92-100.

NIOSH [2002a]. Health hazard evaluation. Custom Products, Inc. Cincinnati, OH: U.S. Department of

Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National

Institute for Occupational Safety and Health, HETA 98-0153-2883.

NIOSH [2002b]. Health hazard evaluation. STN Cushion Company. Cincinnati, OH: U.S.. Department

of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention,

National Institute for Occupational Safety and Health, HETA 2000-0410-2891.

NIOSH [2003a]. 1- and 2-Bromopropane. NIOSH analytical method no. 1025. In: NIOSH Manual of

Analytical Methods, 4th ed. Eller, P.M. and Cassinelli M.E., Ed. Cincinnati, OH: U.S. Department of

Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National

Institute for Occupational Safety and Health, DHHS (NIOSH) Publication No. 94-113. Issue date March

15,2003.

NIOSH [2003b]. Health hazard evaluation. Marx Industries, Inc. Cincinnati, OH: U.S. Department of

Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National

Institute for Occupational Safety and Health, HETA 99-0260-2906.

NTP [2002]. NTP-CERHR expert panel report on the reproductive and developmental toxcity of 1-

bromopropane. Washington, DC: U.S. Department ofHealth and Human Services, National Institutes of

Health, National Institute ofEnvironmental Health Sciences, National Toxicology Program, DHHS

(NTP) Publication No. NTP-CERHR-I-BP-02.

NTP [2004]. NTP-CERHR expert panel report on the reproductive and developmental toxcity of 1-

bromopropane. Center for the Evaluation ofRisks to Human Reproduction. Reproduc Tox 18: 157-188.

24
OSHA [1999]. Nomination of I-bromopropane (1-BP) and 2-bromopropane (2-BP) for testing by the

National Toxicology Program. Washington, DC: Department ofLabor, Directorate ofHealth Standards

Programs, U.S. Occupational Safety and Health Administration, DOL (OSHA).

OSHA [2006]. Permissible exposure limits. 29 CFR 1910.1000. Code ofFederal Regulations.

Washington, DC: U.S. Government Printing Office, Office ofFederal Register.

OSHA [2006]. Respiratory Protection. 29 CFR 1910.134. Code ofFederal Regulations. Washington,

DC: U.S. Government Printing Office, Office ofFederal Register

Park YS, Kim Y, Park DW, Choi SK, Park SH, Moon YH [1997]. An outbreak ofhematopoietic and

reproductive disorders due to solvents containing 2-bromopropane in an electronic factory, South Korea:

epidemiological survey. J Oeeup Health 39: 138-143.

Petroferm [2000]. Technical Bulletin: Lenium RV for asphalt extraction and binder recovery.

http://www.petroferm.com. Issue date July 2000.

Rozman K.K., Doull J. [2002]. Derivation of an occupational exposure limit (OEL) for n-propyl bromide

using an improved methodology. App Oee Env Hyg 17(10):711-716.

Sclar G [1999]. Encephalomyelo-radiculoneuropathy following exposure to an industrial solvent. Clin

Neurol and Neurosurg 101:199-202.

Takeuchi Y, Ichihara G, Kamijima M [1997]. A review on toxicity of2-bromopropane: mainly on its

reproductive toxicity. J Oeeup Health 39:179-191.

Takeuchi T., OkdaH., Nagano K., et at. [2001]. Reproductive and developmental toxicity of 1-

bromopropane in rats. Toxieol Sci 26:222.

Toraason M, Lynch D, DeBord G, Singh N, Krieg E, Butler MA, Toennis C, Nemhauser J [2006]. DNA

damage in leukocytes ofworkers occupationally exposed to I-bromopropane. Mut Res 603:1-14.

Wang, HL; Ichihara, G; Ito, H; Kato, K; Kitoh, J; Yamada, T; Yu, X; Tsuboi, S; Moriyama, Y;

Takeuchi, Y. [2003]. Dose-dependent biochemical changes in rat central nervous system after

12-week exposure to l-bromopropane. Neurotoxic 24:199-206.

WIL Research Laboratories, Inc. [2000]. An inhalation two generation reproductive toxicity study of 1-

bromopropane in rats. WIL-380001. Ashland, OH 44805. Sponsored by the Brominated Solvents

Consortium (BSOC). Available from USEPA docket A-2001-07, document II-D-IO.

Yamada T., Ichihara G., Wang H., Yu X., Maeda K., Tsukamura H., Kamijima M., Nakajima T.,

Takeuchi Y [2003]. Exposure to I-bromopropane causes ovarian dysfunction in rats. Tox Sci 71:96-103.

Yu X, Ichihara G, Kitoh J, Xie Z, Shibata E, Kamijima M, Asaeda N, Hisanaga N, Takeuchi Y [1999].

Effect of inhalation exposure to 2-bromopropane on the nervous system in rats. Toxieol135:87-93.

Yu X, Ichihara G, Kitoh J, Xie Z, Shibata E, Kamajima M, Takeuchi Y [2001]. Neurotoxicity of2-

bromopropane and I-bromopropane, alternative solvents for chlorofluorocarbons. Envir Res 85(1):48-52.

25