HETA 94-0122-2578

Bath Iron Works Corporation

Bath, Maine

David C. Sylvain, M.S., CIH

This Health Hazard Evaluation (HHE) report and any recommendations made herein are for the specific facility evaluated and may not be universally

applicable. Any recommendations made are not to be considered as final statements of NIOSH policy or of any agency or individual involved.

Additional HHE reports are available at http://www.cdc.gov/niosh/hhe/reports

This Health Hazard Evaluation (HHE) report and any recommendations made herein are for the specific facility evaluated and may not be universally

applicable. Any recommendations made are not to be considered as final statements of NIOSH policy or of any agency or individual involved.

Additional HHE reports are available at http://www.cdc.gov/niosh/hhe/reports

This Health Hazard Evaluation (HHE) report and any recommendations made herein are for the specific facility evaluated and may not be universally

applicable. Any recommendations made are not to be considered as final statements of NIOSH policy or of any agency or individual involved.

applicable. Any recommendations made are not to be considered as final statements of NIOSH policy or of any agency or individual involved.

Additional HHE reports are available at http://www.cdc.gov/niosh/hhe/reports
ii

PREFACE

The Hazard Evaluations and Technical Assistance Branch of NIOSH conducts field investigations of possible

health hazards in the workplace. These investigations are conducted under the authority of Section 20(a)(6)

of the Occupational Safety and Health Act of 1970, 29 U.S.C. 669(a)(6) which authorizes the Secretary of

Health and Human Services, following a written request from any employer or authorized representative of

employees, to determine whether any substance normally found in the place of employment has potentially

toxic effects in such concentrations as used or found.

The Hazard Evaluations and Technical Assistance Branch also provides, upon request, technical and

consultative assistance to Federal, State, and local agencies; labor; industry; and other groups or individuals

to control occupational health hazards and to prevent related trauma and disease. Mention of company names

or products does not constitute endorsement by the National Institute for Occupational Safety and Health.

ACKNOWLEDGMENTS AND AVAILABILITY OF REPORT

This report was prepared by David C. Sylvain, M.S., CIH, of the Hazard Evaluations and Technical

Assistance Branch, Division of Surveillance, Hazard Evaluations and Field Studies (DSHEFS). Field

assistance was provided by Mark F. Greskevitch and methods for the analysis of steel shot were developed

by Mark Millson. Desktop publishing by Pat Lovell.

Copies of this report have been sent to employee and management representatives at BIW and the OSHA

Regional Office. This report is not copyrighted and may be freely reproduced. Single copies will be

available for a period of three years from the date of this report. To expedite your request, include a selfaddressed mailing label along with your written request to:

NIOSH Publications Office

4676 Columbia Parkway

Cincinnati, Ohio 45226

800-356-4674

After this time, copies may be purchased from the National Technical Information Service (NTIS) at

5825 Port Royal Road, Springfield, Virginia 22161. Information regarding the NTIS stock number may be

obtained from the NIOSH Publications Office at the Cincinnati address.

For the purpose of informing affected employees, copies of this report shall be

posted by the employer in a prominent place accessible to the employees for a

period of 30 calendar days.
iii

Health Hazard Evaluation Report 94-0122-2578

Bath Iron Works Corporation

Bath, Maine

May 1996

David C. Sylvain, M.S., CIH

SUMMARY

In December 1993, the National Institute for Occupational Safety and Health (NIOSH) received a Health

Hazard Evaluation (HHE) request from Bath Iron Works Corporation (BIW) Occupational Safety and Health

Department, Bath, Maine, to evaluate the accuracy of personal air monitoring conducted during abrasive

blasting in confined spaces. The BIW industrial hygiene staff provided information indicating that abrasive

grit particles enter environmental air sampling cassettes, resulting in an overestimation of worker exposure

to inhalable airborne metals.

 

On March 31, 1994, an opening conference was held and a walk-through evaluation of the abrasive blasting

operation was conducted. On July 19-21, 1994, 15 personal breathing zone (PBZ) air samples were collected

during manual abrasive blasting in confined spaces. A second sample, collected concurrently with each PBZ

sample, was obtained behind each blaster’s head to determine if sample placement had an effect on reducing

the amount of grit entering the cassette. In addition to analysis for lead and selected metals, a visual

assessment of the grit in the cassettes was made. On February 28-March 2, 1995, ten sets of side-by-side

PBZ air samples were collected during abrasive blasting inside a 7' x 4' x 2' steel tank. Each set consisted

of a sample using a standard closed-face cassette; a closed-face cassette fitted with a metal guard to shield

the inlet from high-velocity grit (“grit guard”); and a sample using a 10mm nylon cyclone at a flow rate of

300cc/minute. Prior to sample analysis, the steel grit was separated from the filters and dust in the closedface cassettes; the fractions were analyzed separately. 

Although only low levels of lead and other contaminants were present in the base-metal, surface coating, and

steel grit, the relatively large mass of grit that entered the air sampling cassettes resulted in an overestimation

of the airborne lead concentration. Evaluation of air samples collected during this HHE indicates that

conventional air sampling methods over estimate concentrations of lead and other inhalable airborne

contaminants present in abrasive blasting environments. Use of the metal guard, and locating sampling

cassettes behind the head (or body) were not reliable methods for preventing grit from entering cassettes.

Grit did not penetrate most of the cyclones in the test tank; however, cyclones would not be useful under

actual blasting conditions, because they would be inverted as the blasters climbed through confined spaces.

Neither grit guards or placement of several samples appear to effectively control entrance of abrasive blasting

grit.
iv

Conventional sampling and analytical methods do not provide an accurate estimate of airborne

concentrations of lead and other contaminants present during abrasive blasting in small, confined

spaces. Abrasive grit enters the cassette inlet due its high velocity (inertia), resulting in an

overestimation of actual airborne contaminant concentrations. Neither grit guards or placement of

personal samples appear to effectively control entrance of abrasion blasting grits.

Keywords: SIC 3731 (Ship building and repairing), abrasive blasting, air sampling, elemental metals,

lead. 
TABLE OF CONTENTS

Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ii

Acknowledgments and Availability of Report . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ii

Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iii

Introduction ........................................................................ 2

Background ........................................................................ 2

Methods ........................................................................... 3

Air Samples . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

Bulk Samples . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4

Evaluation Criteria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4

Lead . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

Lead in surface dust and soil .................................................... 6

Lead - childhood exposure ...................................................... 6

Cadmium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

Chromium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8

Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8

Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
Page 2 Health Hazard Evaluation Report No. 94-0122

INTRODUCTION

In December 1993, the National Institute for

Occupational Safety and Health (NIOSH)

received a Health Hazard Evaluation (HHE)

request from Bath Iron Works Corporation (BIW)

Occupational Safety and Health Department,

Bath, Maine. This was a request for assistance in

evaluating the accuracy of sampling methods used

to collect personal air samples during abrasive

blasting in confined spaces. The BIW Industrial

Hygiene Division had collected sampling data

which indicated that large, high-velocity grit

particles enter sampling cassettes, resulting in an

overestimation of worker exposure to lead. 

An accurate estimate of lead exposure is needed to

select appropriate personal protective equipment,

conduct appropriate medical monitoring, and

implement appropriate administrative controls.

The Occupational Safety and Health

Administration (OSHA) lead standard (29 CFR

1910.1025) requires that controls be implemented

if personal exposure monitoring indicates that

employees are exposed to lead concentrations

which exceed the OSHA action level or

permissible exposure limit. The lead standard

prescribes an acceptable level of accuracy for the

sampling and analytical method used to evaluate

workplace exposure to lead. The NIOSH Manual

of Analytical Methods, OSHA compliance

directives, and OSHA instructions provide

guidance on various sampling issues, such as

calibration of sampling pumps, and sampling flow

rate; however, no guidance is provided to address

the issue of large, noninhalable particles found in

samples obtained during abrasive blasting in

confined spaces. Since there is no acceptable

method for removing blasting grit from sampling

cassettes prior to sample analysis, the grit is

included in the analysis. Even a small quantity of

steel grit can result in an overestimate of the

concentration of inhalable lead particulate.

On March 31, 1994, an opening conference was

held and a walk-through evaluation of the abrasive

blasting operation was conducted. Air sampling

was conducted during subsequent site visits on

July 19 - 21, 1994, and February 28 - March 2,

1995. 

BACKGROUND

BIW is a large shipyard on the coast of Maine

which employed approximately 9,000 workers at

the time of this evaluation. Operations at BIW are

primarily involved with the construction of U.S.

Navy Aegis destroyers. The destroyers are

constructed in large sections known as units,

which undergo a sequential construction process

at various locations throughout the shipyard.

When the hull, decks, bulkheads, tanks, and

compartments of a unit have been constructed

from steel plate, the unit is moved into one of two

blast buildings (Blast-1 and Blast-2) where it

undergoes manual abrasive blasting to remove

scale, rust, and zinc-based preconstruction primer.

When structural work is completed, the unit is

transported to the ways where it is hoisted into

place, and assembled with other units.

Construction continues upon the ways, as the ship

is fitted-out in preparation for launching.

Mild and alloy steel plate is used in the

construction; no leaded steel is used. The

abrasive blasting material is angular steel grit

which is collected and reused. The floor of each

blast building consists of a steel grate which

allows used grit to be collected by a mechanical

sweeper system which returns the grit to a

classifier where fines are removed. Fines include

rust, paint, base-steel, and disintegrated grit. Grit

that is deposited in the unit during blasting is

removed by vacuuming. After passing through a

classifier, the grit is returned to the grit pots for

reuse. Grit is periodically replenished with virgin

grit, as disintegrated grit is removed by the

classifier. Blast-1 is equipped with two

classifiers, and Blast-2 has one classifier. General

mechanical ventilation is provided in each blast

building. 
Health Hazard Evaluation Report No. 94-0122 Page 3

Each blast building is equipped with two grit pots,

each of which serves eight blasters. Since all

surfaces must be prepared for painting, the

blasters have to climb over and around baffles,

stiffeners, and other obstacles to reach the tanks,

bilges, and other remote locations within the units.

When blasting in tight spaces, the blaster and air

monitoring equipment are exposed to grit that

rebounds off work surfaces. 

Blasters wear personal protective equipment (ppe)

which includes gloves, boots, coveralls (taped at

the boots), and an MSA® continuous-flow

supplied-air blast hood. Facilities provided at the

site include separate lockers for street and work

clothes, and mandatory showers. Blasters are

required to participate in a medical monitoring

program, which includes physical examinations

and blood-lead monitoring.

METHODS

Air Samples

This evaluation consisted of observation of work

practices (including the use of ppe), and

environmental sampling in the blast buildings. On

July 19-21, 1994, 15 personal breathing zone

(PBZ) air samples were collected during abrasive

blasting inside of two units. A second sample,

collected concurrently with the PBZ sample, was

obtained behind each blaster’s head. Each sample

was obtained using a battery-powered sampling

pump to draw air through a 37 millimeter (mm)

diameter, 0.8 micrometer (μm) pore-size cellulose

ester membrane (MCE) filter mounted in a closedface cassette. The pumps were operated at a

nominal flow rate of 2.0 liters per minute (lpm),

and were calibrated before and after sampling to

ensure that the desired flow rate was maintained

throughout the sampling period. Air samples

were analyzed for lead, and selected elemental

metals, according to NIOSH Method 7300

modified for microwave digestion and standard

matrix matching of samples. Analysis was

performed using a Thermo Jarrell Ash ICAP-61

inductively coupled plasma (ICP) emission

spectrometer controlled by a Digital DEC Station

333c personal computer. Analysis for lead was

repeated according to NIOSH Method 7105

(atomic absorption spectroscopy). In addition, the

analyst provided a visual assessment of the

quantity of grit in the sampling cassettes, and

noted whether there was an appreciable difference

between the amount of grit in PBZ and behindthe-head samples.

On February 28-March 2, 1995, ten sets of sideby-side PBZ air samples were collected during

abrasive blasting inside of a 7' x 4' x 2' steel tank.

Each set of samples consisted of one sample

obtained on a 37 mm diameter, 0.8 μm pore-size

MCE filter mounted in a closed-face cassette; a

second sample was collected using a standard

closed-face cassette which was fitted with a “grit

guard”; and a third sample was collected on a

MCE filter using a 10 millimeter nylon cyclone.

The pumps that were used to collect samples in

closed-face cassettes were operated at a nominal

flow rate of 2.0 lpm. Cyclone samples were

obtained at a nominal flow rate of 300 cubic

centimeters per minute (cc/m) in an attempt to

collect a thoracic cut, i.e., particulate which would

be deposited within the airways and gas-exchange

region of the lung. Each sampling pump was

calibrated before and after sampling to ensure that

the desired flow rate was maintained throughout

the sampling period. 

Prior to analysis, closed-face cassettes were

opened by the analyst, and the steel grit particles

were separated from the dust in each sample using

a rubber-coated magnet. Deionized water was

used to rinse residual dust from the shot into a

beaker containing the filter. The steel grit was

scraped into a separate beaker; and the magnet

was rinsed with 10 percent nitric acid. Air

samples (including cyclone samples) were

analyzed for lead, and selected elemental metals

according to NIOSH Method 7300. 
Page 4 Health Hazard Evaluation Report No. 94-0122

Bulk Samples

On July 20 and 21, 1994, bulk samples of used

abrasive blasting grit, fines, paint (primer), and

base metal (steel) were collected. Grit was

obtained from the bilge of the unit in Blast-1, and

from the grit pots in both blast buildings. A

sample of fines was obtained from classifiers in

each building. Samples of weldable primer and

steel plate were provided by the BIW laboratory.

Bulk samples were analyzed for lead, cadmium,

and arsenic according to NIOSH Method 7300. 

During the 1995 site visit, one sample each of

virgin and used abrasive blasting grit was

collected. Five replicate aliquots of each grit

sample were weighed and then placed in 15 ml

graduated centrifuge tubes. Ten ml of five

percent nitric acid was added to each sample

which was then sonicated for 15 minutes. After

two hours, the leachates were decanted into

separate containers. To each grit residue, 0.5 ml

of a 4% nitric acid-1% perchloric acid solution

was added, and the samples were allowed to stand

at room temperature until complete dissolution

had occurred. The samples were then diluted with

de-ionized water to 10.0 ml final volume, and

were analyzed by ICP-AES. 

EVALUATION CRITERIA

As a guide to the evaluation of the hazards posed

by workplace exposures, NIOSH field staff

employ environmental evaluation criteria for the

assessment of a number of chemical and physical

agents. These criteria are intended to suggest

levels of exposure to which most workers may be

exposed up to 10 hours per day, 40 hours per

week for a working lifetime without experiencing

adverse health effects. It is, however, important to

note that not all workers will be protected from

adverse health effects even though their exposures

are maintained below these levels. A small

percentage may experience adverse health effects

because of individual susceptibility, a pre-existing

medical condition, and/or a hypersensitivity

(allergy). In addition, some hazardous substances

may act in combination with other workplace

exposures, the general environment, or with

medications or personal habits of the worker to

produce health effects even if the occupational

exposures are controlled at the level set by the

criterion. These combined effects are often not

considered in the evaluation criteria. Also, some

substances are absorbed by direct contact with the

skin and mucous membranes, and thus potentially

increase the overall exposure. Finally, evaluation

criteria may change over the years as new

information on the toxic effects of an agent

become available.

The primary sources of environmental evaluation

criteria for the workplace are: (1) NIOSH

Recommended Exposure Limits (RELs)1

, (2) the

American Conference of Governmental Industrial

Hygienists' (ACGIH) Threshold Limit Values

(TLVsTM)2

, and (3) the U.S. Department of Labor,

OSHA Permissible Exposure Limits (PELs)3

.

In July 1992, the 11th Circuit Court of Appeals

vacated the 1989 OSHA PEL Air Contaminants

Standard. OSHA is currently enforcing the 1971

standards which are listed in the current Code of

Federal Regulations; however, some states

operating their own OSHA approved job safety

and health programs continue to enforce the 1989

limits. NIOSH encourages employers to follow

the 1989 OSHA limits, the NIOSH RELs, the

ACGIH TLVs, or whichever are the more

protective criterion. The OSHA PELs reflect the

feasibility of controlling exposures in various

industries where the agents are used, whereas

NIOSH RELs are based primarily on concerns

relating to the prevention of occupational disease.

It should be noted when reviewing this report that

employers are legally required to meet those

levels specified by an OSHA standard and that the

OSHA PELs included in this report reflect the

1971 values.

A time-weighted average (TWA) exposure refers

to the average airborne concentration of a

substance during a normal 8-to-10-hour workday.

Some substances have recommended short-term
Health Hazard Evaluation Report No. 94-0122 Page 5

exposure limits (STEL) or ceiling values which

are intended to supplement the TWA where there

are recognized toxic effects from higher exposures

over the short-term.

Lead

Lead is ubiquitous in U.S. urban environments

due to the widespread use of lead compounds in

industry, gasoline, and paints during the past

century. Exposure to lead occurs via inhalation of

dust and fume, and ingestion through contact with

lead-contaminated hands, food, cigarettes, and

clothing. Absorbed lead accumulates in the body

in the soft tissues and bones. Lead is stored in

bones for decades, and may cause health effects

long after exposure as it is slowly released in the

body. 

Symptoms of lead exposure include weakness,

excessive tiredness, irritability, constipation,

anorexia, abdominal discomfort (colic), fine

tremors, and "wrist drop."4, 5, 6

 Overexposure to

lead may also result in damage to the kidneys,

anemia, high blood pressure, infertility and

reduced sex drive in both sexes, and impotence.

An individual's blood lead level (BLL) is a good

indication of recent exposure to, and current

absorption of lead.7

 The frequency and severity of

symptoms associated with lead exposure generally

increase with the BLL. 

The overall geometric mean BLL for the U.S.

adult population (ages 20-74 yrs) declined

significantly between 1976 and 1991, from 13.1 to

3.0 micrograms per deciliter of blood (μg/dL)--

this decline is most likely due primarily to the

reduction of lead in gasoline. More than 90% of

adults now have a BLL of <10 μg/dL, and more

than 98% have a BLL <15 μg/dL.8

Under the OSHA general industry lead standard

(29 CFR 1910.1025), the PEL for airborne

exposure to lead is 50 μg/m3

 (8-hour TWA).3 The

standard requires lowering the PEL for shifts

exceeding 8 hours, medical monitoring for

employees exposed to airborne lead at or above

the action level of 30 μg/m3

 (8-hour TWA),

medical removal of employees whose average

BLL is 50 μg/dL or greater, and economic

protection for medically removed workers.

Medically removed workers cannot return to jobs

involving lead exposure until their BLL is below

40 μg/dL. The OSHA interim final rule for lead

in the construction industry (29 CFR 1926.62)

provides an equivalent level of protection to

construction workers. ACGIH has adopted a TLV

for lead of 50 μg/m3

 (8-hour TWA), with worker

BLLs to be controlled to at or below 30 μg/dL,

and designation of lead as an animal carcinogen.2

The U.S. Public Health Service has established a

goal, by the year 2000, to eliminate all

occupational exposures that result in BLLs greater

than 25 μg/dL.9

 

The occupational exposure criteria (above) are not

protective for all the known health effects of lead.

For example, studies have found neurological

symptoms in workers with BLLs of 40 to

60 μg/dL, and decreased fertility in men at BLLs

as low as 40 μg/dL. BLLs are associated with

increases in blood pressure, with no apparent

threshold through less than 10 μg/dL. Fetal

exposure to lead is associated with reduced

gestational age, birth weight, and early mental

development with maternal BLLs as low as 10 to

15 μg/dL.10 Men and women who are planning on

having children should limit their exposure to

lead. 

In homes with a family member occupationally

exposed to lead, care must be taken to prevent

"take home" of lead, that is, lead carried into the

home on clothing, skin, and hair, and in vehicles.

High BLLs in resident children, and elevated

concentrations of lead in house dust, have been

found in homes of workers employed in industries

associated with high lead exposure.11 Particular

effort should be made to ensure that children of

persons who work in areas of high lead exposure

receive a BLL test.
Page 6 Health Hazard Evaluation Report No. 94-0122

Lead in surface dust and soil

Lead-contaminated surface dust and soil represent

potential sources of lead exposure, particularly for

young children. This may occur either by direct

hand-to-mouth contact, or indirectly from hand-tomouth contact with contaminated clothing,

cigarettes, or food. Previous studies have found a

significant correlation between resident children’s

BLLs and house dust lead levels.12 There is

currently no federal standard which provides a

permissible limit for lead contamination of

surfaces in occupational settings. As required by

Section 403 of the Toxic Substances Control Act

(TSCA), EPA is in the process of developing a

rule to address hazards from lead-contaminated

dust and soil in and around homes. 

EPA currently recommends the following

clearance levels for surface lead loading be

met after residential lead abatement or interim

control activities: uncarpeted floors,

100 micrograms per square foot (μg/ft2

); interior

window sills, 500 μg/ft2

, and window wells, 800

μg/ft2

.

13 These levels have been established as

achievable through lead abatement and interim

control activities, and they are not based on

projected health effects associated with specific

surface dust levels. 

EPA currently recommends a strategy of scaled

responses to soil lead contamination, depending

upon lead concentrations and site-specific factors.

When lead concentrations exceed 400 ppm in bare

soil, EPA recommends further evaluation and

exposure reduction activities be undertaken,

appropriate to the site-specific level of risk. If soil

lead concentrations exceed 5000 ppm, EPA

recommends permanent abatement of

contaminated soil.13

Lead-childhood exposure

The adverse effects of lead on children and

fetuses include decreases in intelligence and brain

development, developmental delays, behavioral

disturbances, decreased stature, anemia, decreased

gestational weight and age, and miscarriage or

stillbirth. Lead exposure is especially devastating

to fetuses and young children due to potentially

irreversible toxic effects on the developing brain

and nervous system.10

No threshold has been identified for the harmful

effects of lead in children; the Centers for Disease

Control and Prevention (CDC) currently

recommends a multitier approach to defining and

preventing childhood lead poisoning, based on

BLL screening.14 The BLLs and corresponding

actions which CDC has recommended are: $10

μg/dL, community prevention activities; $15

μg/dL, individual case management including

nutritional and educational interventions and more

frequent screening; $20 μg/dL, medical

evaluation, environmental investigation and

remediation. Additionally, environmental

investigation and remediation are recommended

for BLLs of 15-19 , if such levels persist. 

Overall, U.S. population blood lead levels have

declined since 1976. A recent national survey

found that the geometric mean BLL for children

ages 1-11 ranged from 2.5-4.1 μg/dL, with the

highest mean BLL among children aged 1-2

years.15 However, it was estimated from the

survey that 8.9% of U.S. children under 6 years,

or about 1.7 million children, have elevated BLLs

($ 10 μg/dL).

Cadmium

Cadmium is a toxic heavy metal used in the

manufacture of batteries, pigments, and jewelry,

and as a neutron absorber in nuclear reactors.

Cadmium may enter the body either by ingestion

(swallowing) or by inhalation (breathing) of

cadmium metal or oxide. Approximately 6 to

10% of ingested cadmium and 15 to 30% of

inhaled cadmium is absorbed into the body.16

Cadmium is transported from the site of

absorption by the red blood cells and plasma. It is

deposited in organs throughout the body, but

major depositions occur in the liver and kidneys.

Under normal conditions, the kidneys accumulate
Health Hazard Evaluation Report No. 94-0122 Page 7

the greatest concentrations of cadmium.

Cadmium is excreted from the body only very

slowly, and thus accumulates in the cortex of the

kidneys over a lifetime. The blood cadmium

concentration is the best biological indicator of

recent cadmium exposure and absorption.17,18 The

normal blood cadmium level is below 0.7 μg/dL.

Chronic cadmium exposure can be assessed by

measuring the cadmium content of the kidneys

through the technique of neutron activation

analysis.19 The urine cadmium concentration,

although used widely as an index of exposure, is

primarily an indicator of cadmium-induced kidney

damage; the urine cadmium concentration does

not ordinarily begin to increase until after injury

has occurred to the kidneys.20

Acute inhalation exposure to cadmium can cause

pneumonia or pulmonary edema,21 as well as liver

and kidney damage.22 Ingestion of toxic quantities

can produce nausea, vomiting, and diarrhea.

Exposure to an airborne concentration of 50

mg/m3

 cadmium dust is considered immediately

dangerous to life.

Occupational exposure to cadmium is usually

chronic. Chronic occupational exposure to

cadmium can produce toxic effects, including

emphysema of the lungs and chronic kidney

disease.16 Kidney disease, resulting from

cadmium exposure, is a principal concern.16

Although much remains to be learned about the

development of kidney disease in persons exposed

to cadmium, the process appears to be a gradual

one.20 Also, the process is dose-related; persons

with greatest lifetime absorption of cadmium are

at greatest risk of kidney disease (nephropathy).

The initial signs of cadmium nephropathy are

subtle--affected workers will usually have no

symptoms in the early stages, and their kidney

function test results may still be within the broad

range of normal, although their test results will

tend over time to move toward the high end of the

normal range.

Because the kidney has an enormous reserve

capacity, results of the usual renal function

tests--blood urea nitrogen (BUN), serum

creatinine, and serum uric acid--will not become

frankly abnormal until one-third to one-half of

kidney function has been destroyed.23 For that

reason, more sensitive screening tests of renal

function have been sought. These include

measurement of serum concentrations of

l,2,5-dihydoxy vitamin D (which may be

decreased),24 and measurement of urine

concentrations of cadmium and of protein

beta-2-microglobulin (both of which are reported

to increase in persons with kidney damage caused

by cadmium).25 Also, aminoaciduria, renal

glycosuria, or hyperphosphaturia may develop.

When any of these test results are abnormal in a

person exposed to cadmium, or even when two or

more test results are in the high normal range,

there exists a possibility of kidney damage. In

that circumstance, more complete evaluation of

the worker by a kidney disease specialist is

required.

Occupational cadmium exposure has been

associated with cancer of the prostate gland.26 In

1976, a NIOSH study of workers in a cadmium

production factory provided limited evidence that

occupational cadmium exposure may be

associated with lung cancer.27 Subsequent to the

1976 report, the cohort was expanded from the

original 292 workers to 602 white males who had

worked at least six months between 1940 and

1969 in the cadmium production area of the

cadmium smelting plant28 In this study, the

mortality from cancer of the respiratory tract was

significantly greater in the entire cohort than

would have been expected from rates in the

general U.S. population. This study found that

lung cancer mortality increased with increasing

cumulative exposure to cadmium. 

Under the OSHA general industry cadmium

standard (29 CFR 1910.1027), the PEL for

airborne exposure to cadmium is 5 μg/m3

,

calculated as an 8-hour TWA. The standard

requires medical monitoring for employees

exposed to airborne cadmium at or above the
Page 8 Health Hazard Evaluation Report No. 94-0122

action level of 2.5 μg/m3 (8-hour TWA); and

requires medical removal of employees based

upon the physician’s determination. The OSHA

final rule for cadmium in the construction industry

(29 CFR 1926.63) provides an equivalent level of

protection for construction workers.29 ACGIH has

adopted a TLV for cadmium of 0.01 μg/m3

 (8-

hour TWA) for inhalable (total) dust/particulate;

and 0.002 μg/m3

 for the respirable fraction.

NIOSH classifies cadmium as a potential

occupational carcinogen, and recommends that

occupational exposures be reduced to the "lowest

feasible level" (LFL) because it is not possible to

establish thresholds for carcinogens which will

protect 100% of the population.

Chromium

Chromium (Cr) exists in a variety of chemical

forms, and toxicity varies among the different

forms. For example, elemental chromium is

relatively non-toxic.30 The PEL for chromium

metal is an 8-hour TWA concentration of 1

mg/m3

. The ACGIH TLV, and NIOSH REL for

chromium metal, and chromium (II) and

chromium (III) compounds, is 0.5 mg/m3

.

Other chromium compounds may cause skin

irritation, sensitization, and allergic dermatitis. In

the hexavalent form (Cr(VI)), Cr compounds are

corrosive, and possibly carcinogenic. Until

recently, the less water-soluble Cr(VI) forms were

considered carcinogenic while the water-soluble

forms were not considered carcinogenic. Recent

epidemiological evidence indicates

carcinogenicity among workers exposed to soluble

Cr(VI) compounds.31,32,33,34,35 Based on this

evidence, NIOSH recommends that all Cr(VI)

compounds be considered as potential

carcinogens. 

RESULTS

Air samples collected on July 19 - 21, 1994, were

analyzed for inorganic arsenic, lead, and cadmium

according to NIOSH Method 7300 (inductively

coupled plasma-atomic emission spectroscopy).

Due to high iron content in the samples, numerous

dilutions were required to eliminate spectral

saturation interferences. As a consequence, the

analytical limits of detection and quantitation

were increased up to forty times the limits listed

for this method, thus rendering this analysis

insensitive and unreliable. Analysis for lead and

elemental chromium was repeated according to

NIOSH Methods 7105 (atomic absorption

spectroscopy) and 7300 respectively. Analysis for

elemental chromium was initiated by the

laboratory due to high chromium concentrations

detected during the first analysis. Results of the

repeat analysis are presented in Table 1. For sideby-side samples where the quantity of grit in each

cassette could be visually assessed, analysis of the

air sample filters (and loose grit) revealed that the

cassette containing the greatest amount of grit

generated results indicating the highest air

contaminant concentration. The exception to this

observation in sample set P12 - BH12, appears to

be due to the marked difference between the

sample volumes for P12 and BH12 (212 L vs. 4.82

L). 

Analysis of bulk samples of used grit collected

during the July 1994 visit revealed concentrations

of elemental lead, cadmium, and arsenic in the

range of 43 to 50 μg/g (Table 2; samples K23 -

K25). The lead content of classifier fines

appeared to be somewhat higher than in the grit;

while the arsenic concentration in the fines was

less than that in grit samples. Forty to 97 μg/g

lead was detected in paint and base-metal

samples. No arsenic was detected in paint or

base-metal samples; cadmium concentrations in

these samples were less than was found in grit.

Results of air samples collected on February 28

through March 2, 1995, are presented in Table 3.
Health Hazard Evaluation Report No. 94-0122 Page 9

Eight samples exceeded the OSHA PEL for lead

when the steel grit fraction was included in the

calculation of the 8-hour TWA concentration.

Four of the 8 samples exceeded the OSHA PEL

for elemental chromium when the steel grit

fraction was included. None of the results

exceeded the PELs if the contribution of the grit

fraction was not included. The minimum

quantifiable concentration (MQC) for all of the

cadmium analyses was greater than the OSHA

PEL; therefore, cadmium results could not be

evaluated in terms of the OSHA cadmium

standard, 29 CFR 1910.1027. Similarly, the MQC

for arsenic analyses was greater than the REL

and/or PEL; and, as a consequence, the air

sampling conducted for arsenic during this visit

could not be evaluated with respect to these limits.

Analysis of surface dust, extracted from bulk

samples of abrasive blasting grit, determined that

lead and cadmium concentrations in the dust were

below the analytical limit of quantitation (LOQ)

(Table 4). Dissolution and analysis of virgin grit

(after extraction of surface dust) detected average

lead and cadmium concentrations of 115 μg/g, and

15.4 μg/g respectively. Dissolution and analysis

of used grit determined the average lead and

cadmium content of used grit to be 90.8 μg/g and

24.5 μg/g.

DISCUSSION

In the absence of guidelines for the analysis of

non-inhalable particles, all dust and grit is

digested, analyzed, and reported as airborne

contaminant(s): in this case, lead and selected

elemental metals. Analysis of side-by-side air

samples obtained during manual abrasive blasting

in July 1994, appears to support the supposition

that analysis of steel grit found in sample cassettes

contributes substantially to sampling results: as

expected, the analysis revealed that the cassette

which contained the greater quantity of grit

generated a higher estimate of airborne lead

concentration than did the corresponding sample.

This observation was based on a visual

comparison of the quantity of grit inside of paired

cassettes in relation to analytical results. This

analysis did not attempt to distinguish between

particulate that was collected on the filter, dust on

the surface of the grit, and the contaminants which

comprise the steel grit itself. Figure 1 shows an

open cassette with grit that accumulated during

abrasive blasting sampling. 

Bulk samples had similar lead concentrations in

the base metals, zinc-based primer, and used grit.

The highest concentration of lead (97μg/g) was in

steel used to construct internal stiffeners, which

comprise little of the surface area within the units.

Although the composition of the grit was similar

to that of the base metals and primer, much more

grit entered the sample cassettes during sampling

than did primer or base metals. Thus, the factor

which appeared to have the greatest impact on

sample results was the amount of grit in the

cassettes, and the lead contamination contributed

by the grit.

The intent of paired samples (PBZ and behind the

head), was to obtain a qualitative assessment of

the effect of “shielding” the cassette from

rebounding grit. The PBZ sample contained more

grit in five sets; the behind-the-head sample

contained more grit in two sets; and the amount of

grit was determined to be essentially the same in

one sample set. These results indicate that

locating the cassette behind the head (or body) is

not a reliable method of preventing rebounding

grit from entering sampling cassettes. The space

within tanks, bilges, etc. is extremely small, and

grit enters the cassettes regardless of location. 

Difficulties encountered during sampling included

equipment and sampling train damage/failure; and

sample overloading. The sampling train was often

damaged as the workers moved over, under, and

around obstacles within the units. Damage

included broken cassettes, torn Tygon tubing, and

detached pump belt clips. Due to the

inaccessibility of the work areas, it was not

possible to change cassettes to prevent cassettes
Page 10 Health Hazard Evaluation Report No. 94-0122

from becoming overloaded with grit. 

During the 1995 visit, sampling was conducted

inside of a tank that the BIW Industrial Hygiene

Division had constructed for the purpose of

collecting sampling data. The tank provided a

relatively uniform, controlled environment in

which sampling could be conducted with minimal

sample loss. The tank was constructed of the

same grade of steel as the units, and was primed

with the same zinc-based primer prior to blasting.

Unlike actual spaces within the units, this tank

allowed the blaster to remain in an upright

position, and allowed for collection of samples

using nylon cyclones. Cyclones could not be used

because they would be inverted as the blasters

climbed through the units.

Most cyclone sampling results approximated the

filter and dust results that were obtained using

closed-face cassettes. Grit did not penetrate most

cyclones; however, sample 3C contained only

steel grit and no dust. The absence of dust in this

sample was due to failure of the sampling pump

after 7 minutes of sampling. Although the pumps

were operated at 300cc/min in an attempt to

collect a thoracic cut, it is not known if this size

range was actually collected. Thus, it is not

possible to evaluate the performance of the

cyclones in the test tank. However, if cyclones

performed satisfactorily in a test environment,

they could not be used in the units. 

Side-by-side sampling was conducted using a

conventional closed-face cassette; a conventional

closed-face cassette fitted with a “grit guard;” and

a 10mm nylon cyclone operated at a flow rate of

300cc/minute. (A grit guard is a metal guard,

developed by BIW, that clips onto a closed-face

cassette to shield the inlet from high-velocity

abrasive grit.) Because the grit in the cassettes

was not weighed, the effectiveness of the grit

guard could not be ascertained directly. Using

lead-content (μg/sample) as a benchmark, 8 of 10

sample sets had less grit in the cassette when

fitted with the grit guard than in the conventional

closed-face cassette. However, in three of these

sample sets, chromium analysis produced

contradictory results. 

Prior to the second round of sampling, attempts

were made to identify a size-selective sampler that

could be used in the presence of high-velocity grit

in the blast environment. When an appropriate

size-selective sampler could not be identified, a

method for separating grit from the samples was

proposed. The initial method specified the use of

a 100 μm sieve to separate large particles from

filters and dust. However, when none of the grit

would pass through the sieve, the use of the sieve

was discontinued, and a rubber-coated magnet

was used to remove steel grit. Grit, similar to the

grit shown in figure 1, was removed from the

samples using the magnet.

Separation of grit from filters and dust provided

further evidence that steel grit in the cassettes

produced results which overestimated the actual

concentrations of airborne lead and other metals.

In 18 of the 21 samples where lead was present,

only the grit fraction produced results above the

LOQ. In eight samples, the 8-hour TWA

concentration exceeded the lead PEL when grit

was included; however, results were below the

LOQ when the grit fraction was not included in

the calculation. 

 

Analysis of bulk samples of virgin and used grit

indicated that it is the grit, not dust on the surface

of the grit, that contributes the greatest amount of

lead and other metals. Analysis of dust, which

was extracted (removed) from the surface of used

and virgin grit, revealed that lead and cadmium

concentrations in the dust were below the LOQ

(10 μg/g). The composition of used and virgin

grit appeared to differ with respect to lead,

cadmium and chromium. It is possible that these

samples represent grit from different

manufacturers, or grit from different lots. 
Health Hazard Evaluation Report No. 94-0122 Page 11

CONCLUSIONS

The current NIOSH sampling and analytical

method(s) does not accurately represent worker

exposure to lead and other elements during

abrasive blasting in small, confined spaces. This

inaccuracy arises as the result of abrasive blasting

grit which enters the cassette inlet due to its high

velocity (inertia), rather than being collected on

the filter as an airborne contaminant in an air

sample of known volume. In the absence of

guidelines for the analysis and interpretation of

non-inhalable particle sampling data, all dust and

grit is digested, analyzed, and reported as an

airborne contaminant (in this case, lead and

elemental metals). The sampling conducted

during this HHE indicates that accumulations of

steel grit in sampling cassettes can produce results

which overestimate the concentration of inhalable

lead particulate. Sampling conducted during this

HHE points to the need for a sampling analytical

method that can provide an accurate estimate of

airborne exposure to lead and other elements

during abrasive blasting.

REFERENCES

1. 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, National Institute for

Occupational Safety and Health, DHHS (NIOSH)

Publication No. 92-100.

2. ACGIH [1995]. 1995-1996 threshold limit

values for chemical substances and physical

agents and biological exposure indices.

Cincinnati, OH: American Conference of

Governmental Industrial Hygienists.

3. Code of Federal Regulations [1993]. 29

CFR 1910 Washington, DC: U.S. Government

Printing Office, Federal Register.

4. Hernberg S, et al. [1988]. Lead and its

compounds. In: Occupational medicine. 2nd ed.

Chicago, IL: Year Book Medical Publishers.

5. Landrigan PJ, et al. [1985]. Body lead

burden: summary of epidemiological data on its

relation to environmental sources and toxic

effects. In: Dietary and environmental lead:

human health effects. Amsterdam: Elsevier

Science Publishers.

6. Proctor NH, Hughes JP, Fischman ML

[1991]. Lead. In: Chemical hazards of the

workplace. 3rd ed. Philadelphia, PA: J.B.

Lippincott Company, Philadelphia, pp 353-357.

7. NIOSH [1978]. Occupational exposure to

inorganic lead. Cincinnati, OH: U.S. Department

of Health, Education, and Welfare, Public Health

Service, Centers for Disease Control, National

Institute for Occupational Safety and Health,

DHEW (NIOSH) Publication No. 78-158.

8. Pirkle JL, et al. [1994]. The decline in

blood lead levels in the United States, the

National Health and Nutrition Examination

Surveys (NHANES), JAMA, 272:284-291.

9. DHHS [1990]. Healthy people 2000:

national health promotion and disease objectives.

Washington, DC: U.S. Department of Health and

Human Services, Public Health Service, DHHS

Publication No. (PHS) 91-50212.

10. ATSDR [1990]. Toxicological profile for

lead. Atlanta, GA: U.S. Department of Health and

Human Services, Public Health Service. Agency

for Toxic Substances and Disease Registry.

DHHS (ATSDR) Publication No. TP-88/17.

11. Grandjean P and Bach E [1986]. Indirect

exposures: the significance of bystanders at work

and at home. Am Ind Hyg Assoc J 47(12):819-
Page 12 Health Hazard Evaluation Report No. 94-0122

824.

12. Farfel MR and Chisholm JJ [1990]. Health

and environmental outcomes of traditional and

modified practices for abatement of residential

lead-based paint. American Jour of Pub Health,

80:10, 1240-1245.

13. EPA [1994]. Guidance on residential leadbased paint, lead-contaminated dust, and leadcontaminated soil. Washington, DC: U.S.

Environmental Protection Agency, Office of

Prevention, Pesticides and Toxic Substances.

Memorandum from Lynn Goldman, Assistant

Administrator, July 14, 1994.

14. CDC [1991]. Preventing lead poisoning in

young children: a statement by the Centers for

Disease Control - October 1991. Atlanta, GA:

U.S. Department of Health and Human Service,

Public Health Service, Centers for Disease

Control.

15. Brody DJ, et al. [1994]. Blood lead levels

in the US population, phase 1 on the third

National Health and Nutrition Examination

Survey (NHANES III, 1988 to 1991). JAMA

272:277-283.

16. Webb M: Cadmium. Br Med Bull

1975;31:246-50.

17. Lauwerys R, Roels H, Regniers M, et al.

Significance of cadmium concentration in blood

and in urine in workers exposed to cadmium.

Environ Res 1979;20:375-91.

18. Kjellstrom T. Exposure and accumulation

of cadmium in populations from Japan, the United

States, and Sweden. Environ Health Perspect

1979;28:169-97.

19. Ellis KJ, Vartsky D, Zanai I, et al.

Cadmium: in vivo measurement in smokers and

nonsmokers. Science 1979;205:323-25.

20. Friberg L, Piscator M, Nordberg GF, et al.

Cadmium in the environment. Cleveland: CRC

Press, 1974.

21. Baker EL, Peterson WA, Holtz J, Coleman

C, Landrigan PJ. Subacute cadmium intoxication

in jewelry workers: an evaluation of diagnostic

procedures. Arch Environ Health 1979;34:173-

77.

22. Scott R, Paterson PJ, Mills EA, et al.

Clinical and biochemical abnormalities in

coppersmiths exposed to cadmium. Lancet

1976;2:396-98.

23. Page LB, Culver PJ. A syllabus of

laboratory examinations in clinical diagnosis.

Cambridge: Harvard University Press, 1962.

24. Rosen JF, Chesney R, Hamstra A, DeLuca

H, Mahaffey K. Reduction in 1,25-

dihydroxyvitamin D in children with increased

lead absorption. N Engl J Med 1980;302:1128-

31.

25. Kazantzis G. Renal tubular dysfunction and

abnormalities of calcium metabolism in cadmium

workers. Environ Health Perspect 1979;28:155-

59.

26. Piscator M. Role of cadmium in

carcinogenesis with special reference to cancer of

the prostate. Environ Health Perspect

1981;40:107-20.

27. Lemen RA, Lee JS, Wagoner JK, et al.

Cancer mortality among cadmium production

workers. Ann NY Acad Sci 1976;271:273-79.

28. Thum MJ, Schnorr TM, Smith AB, Halperin

WE, Lemen RA. Mortality among cadmium

production workers - an update. Journal of the

Nat Cancer Inst 1985;2:325-333.

29. Code of Federal Regulations [1993]. 29

CFR 1926 Washington, DC: U.S. Government

Printing Office, Federal Register.
Health Hazard Evaluation Report No. 94-0122 Page 13

30. Proctor NH, Hughes JP, Fischman ML

[1988]. Chemical hazards of the workplace, 2nd

ed. Philadelphia, PA: J.B. Lippincott.

31. Blair A, Mason TJ [1980]. Cancer

mortality in the united States counties with

electroplating industries. Arch Environ Health

35(2):92-94.

32. Franchini I, Magnani F, Mutti A [1983].

Mortality experience among chrome plating

workers: initial findings. Scand J Work Environ

Health 9:247-252.

33. Royle H [1975]. Toxicity of chromic acid

in the chromium plating industry. Environ Res

10:39-53.

34. Silverstein M, Mirer F. Kotelchuck D,

Silverstein B, Bennett M [1981]. Mortality

among workers in a die-casting and electroplating

plant. Scand J Work Environ Health 7 (suppl.

4):156-165.

35.Sorahan T, Burges DCL, Waterhouse JAH

[1987]. A mortality study of nickel\chromium

platers. Br J Ind Med 44:250-258.
Page 14 Health Hazard Evaluation Report No. 94-0122

Table 1. Personal Air Sampling. Bath Iron Works, July 19-21, 1994

sample

number

sample 

period

(minutes)

sample

volume

(liters)

Pb

(mg/m3

)

Cr

(mg/m3) grit

P1 123 245 0.0045 1.1

BH1 malfunction

P2 116 230 0.043 10. P2>BH2

BH2 109 218 0.0046 0.26

P3 139 267 0.012 0.17

BH3 125 206 0.028 8.3 BH3>P3

P4 49 109 0.12 16.

BH4 48 107 0.24 42. BH4>P4

P5 45 104 0.11 7.6 P5>BH5

BH5 45 110 0.072 0.49

P6 11 23.6 (0.003) (0.03)

BH6 83 195 0.033 0.14 BH6>P6

P7 malfunction

BH7 58 140 0.031 1.9

P9 75 167 0.090 3.4 P9=BH9

BH9 75 167 0.066 1.6

P10 75 173 0.098 7.5 P10>BH10

BH10 75 184 0.060 1.7

P11 75 179 0.030 3.5 P11>BH11

BH11 75 176 0.017 0.40

P12 87 212 0.90 12. P12>BH12

BH12 2 4.82 7.1 100.

P13 127 283 0.064 1.3

BH13 malfunction

P14 80 184 0.14 7.1

BH14 malfunction

P15 46 99.8 0.30 34. P15>BH15

BH15 83 195 0.092 2.8

P16 82 204 0.020 1.8 P16>BH16

BH16 82 197 0.011 0.13

mg/m3 = milligrams of contaminant per cubic meter of air

( ) = Value is between the minimum detectable concentration (MDC) and minimum quantifiable concentration (MQC).

 For Pb analysis of this sample, this range is 0.002 - 0.0064 mg/m3; for Cr, 0.01 - 0.04 mg/m3.

> = greater than.

P = Sampling cassette was located in the personal breathing zone.

BH = Sampling cassette was located behind the blaster’s head.
Health Hazard Evaluation Report No. 94-0122 Page 15

Table 2. Bulk Samples, Elemental Analysis. Bath Iron Works (HETA 94-0122), July 19-20, 1994

# material building/location corresponding air samples

Concentration 

(μg/g)

Pb Cd As

K-23 grit Blast-2/bilge P1, P2, P3, BH2, BH3 46. 45. 43.

K-24 grit Blast-1/grit pot P13, P14, BH13, BH14 50. 44. 47.

K-25 grit Blast-2/grit pot P11, P12, BH11, BH12 45. 44. 44.

K-26 fines Blast-1/classifier P13, P14, BH13, BH14 71. 39. 38.

K-27 fines Blast-2/classifier P11, P12, BH11, BH12 72. 50. 31.

L28 primer1 all surfaces all 54. 2.2 <0.5

S29 steel2 internal stiffeners all 97. 4.3 <0.6

S30 steel2 decks, bulkheads all 40. 2.7 <0.5

μg/g = Micrograms of contaminant per gram of bulk sample.

1. Liquid sample of weldable primer. 

2. Sample of the same grade of steel comprising the surfaces being blasted.
Health Hazard Evaluation Report No. 94-0122

al Air Sampling. Bath Iron Works (HETA 94-0122), February 28-March 2, 1995.

sample

period

(minutes)

sample

volume

(liters)

Filter & Dust

(mg/m3) 

Steel Grit2,3

(mg/m3)

Pb Cd As Cr Fe Pb Cd Cr Fe

85 173 nq nq7 nq5 0.027 16.9 0.6658 nq7 3.28 >200.

84 172 nq nq7 nq5 0.017 10.7 0.6058 nq7 7.628 >200.

86 26.6 nq nq7 nq7 0.29 18.7 -- -- -- --

59 120 nq nq7 nq7 0.033 18.3 0.359 nq7 5.57 >200.

14 28.7 nq nq7 nq7 0.08 46.7 0.320 nq7 4.46 >300.57 17.1 nq nq7 nq7 0.11 55.5 -- -- -- --

46 93.8 nq nq7 nq7 0.10 65.5 0.8548 nq7 12.38 >300.

47 94.9 nq nq7 nq7 0.047 27.2 1.8 nq7 3.97 >300.

7 2.14 -- -- -- -- -- 5.758 nq7 75.08 >3000.

63 127 nq nq7 nq5 0.016 12.1 0.119 nq7 1.24 >80.

22 45.3 nq nq7 nq7 0.035 31.3 nq nq7 nq >200.

63 19.2 nq nq7 nq7 0.130 77.3 -- -- -- --

83 173 nq nq7 nq5 0.044 34. 0.3478 nq7 4.9 >200.

83 171 nq nq7 nq5 0.063 38. 0.022 nq7 0.191 >60.

85 25.6 nq nq7 nq7 0.051 29. -- -- -- --

68 141 nq nq7 nq5 0.018 11.9 0.16 nq7 2.11 >70.

68 137 nq nq7 nq5 0.055 31. 0.017 nq7 0.244 >70.

68 20.7 nq nq7 nq7 nq 26.8 -- -- -- --

62 128 nq nq7 nq5 0.011 10. 0.138 nq7 1.59 >80.

46 94.8 nq nq7 nq7 0.021 17.2 0.261 nq7 3.15 >100.42 12.8 nq nq7 nq7 nq 10.4 -- -- -- --
al Air Sampling. Bath Iron Works (HETA 94-0122), February 28-March 2, 1995.

sample

period

(minutes)

sample

volume

(liters)

Filter & Dust

(mg/m3) 

Steel Grit2,3

(mg/m3

)

Pb Cd As Cr Fe Pb Cd Cr Fe

Health Hazard Evaluation Report No. 94-0122

68 139 nq nq7 nq5 0.029 18. 0.264 nq7 3.71 >70.

69 140 nq nq7 nq5 0.066 39.6 0.019 nq7 0.173 >70.

68 20.8 nq nq7 nq7 0.063 28.3 -- -- -- --

55 110 nq nq7 nq7 0.044 23. 0.9458 nq7 10.38 >300.

66 134 0.057 nq7 nq5 0.557 >96.3 0.057 nq7 0.426 >70.

55 17.0 0.059 nq7 nq7 0.270 95.8 -- -- -- --

5 10.3 nq7 nq7 nq7 0.330 240. 8.988 nq7 6.98 >3000.

65 132 0.045 nq7 nq5 0.564 >97.7 0.239 nq7 3.82 >200.

5 1.52 nq7 nq7 nq7 nq5 28.2 -- -- -- --

ms of contaminant per cubic meter of air

antified. Analytical results are reported in terms of the minimum quantifiable concentration (MQC). The MQC for samples with numbers ending in "A" or "B" ranges from 0.007 

mg/m3 for cadmium in the steel grit fraction; and 0.0069 to 0.12 mg/m3 for all other analyses. The MQC for cyclone samples ("C" samples) ranges from 0.02 to 0.4 mg/m3 for lead 

s; and from 0.045 to 0.79 mg/m3 for all other analyses.

s of side-by-side samples were obtained: samples identified with numbers ending in "A" were obtained using a closed-face cassette in the breathing zone; "B" samples were obtained 

closed-face cassette fitted with a "grit guard"; and "C" samples were obtained using a 10 mm nylon cyclone operated at a nominal flow rate of 300 cc/minute. 

 analysis could not be accomplished on the steel grit sample solutions due to spectral interference caused by high iron content. 

it did not penetrate most cyclones; however, sample 3C contained only large particles of grit and no dust.

 of steel grit may have been imbedded in the filter. 

 REL PEL both (REL, PEL)

HA PEL is exceeded when this value is included in the calculation of the 8-hour time-weighted average concentration.
Page 18 Health Hazard Evaluation Report No. 94-0122

 Table 4. Bulk Samples, Elemental Analysis. Bath Iron Works (HETA 94-0122), March 2, 1995

 Sample 1

Concentration 

(μg/g)

Pb Cd Cr Fe

Virgin grit

K1-A extracted surface dust

dissolved grit

<10.0

126.

<10.0

15.6

30.2

698.

 42100

 >150000

K1-B extracted surface dust

dissolved grit

<10.0

109.

<10.0

15.8

62.5

745.

 8183

 >150000

K1-C extracted surface dust

dissolved grit

<10.0

125.

<10.0

16.3

29.5

802.

 48400

 >150000

K1-D extracted surface dust

dissolved grit

<10.0

118.

<10.0

15.0

36.3

655.

 47900

 >150000

K1-E extracted surface dust

dissolved grit

<10.0

96.0

<10.0

14.3

25.5

606.

 49800

 >150000

Used grit

K2-A extracted surface dust

dissolved grit

<10.0

93.7

<10.0

20.9

51.4

1150

 45600

 >150000

K2-B extracted surface dust

dissolved grit

<10.0

95.3

<10.0

22.7

38.0

1040

 41300

 >150000

K2-C extracted surface dust

dissolved grit

<10.0

88.4

<10.0

21.4

69.1

1230

 46400

 >150000

K2-D extracted surface dust

dissolved grit

<10.0

94.6

<10.0

33.0

49.7

1480

 39300

 >150000

K2-E extracted surface dust

dissolved grit

<10.0

82.0

<10.0

24.6

80.9

1330

 56600

 >150000

 μg/g= Micrograms of contaminant per gram of bulk sample.

 1. Samples K1 and K2 were divided into five replicate aliquots identified as A through E.
Page 19 Health Hazard Evaluation Report No. 94-0122

 Table 5. Occupational Exposure Criteria. Bath Iron Works (HETA 94-0122)

Substance NIOSH (REL)

 (mg/m3

)

OSHA (PEL)

 (mg/m3)

Arsenic (As) C 0.002, (Ca) 0.01

Cadmium (Cd) (Ca) 0.005

Chromium metal (Cr) 0.5 1.

Iron Oxide (Fe2O3)

 (as Fe)

 5. 10.

Lead (Pb) 0.1 0.05

All exposure criteria expressed as Time-Weighted Average (TWA) concentrations unless otherwise indicated.

mg/m3 = milligrams of contaminant per cubic meter of air.

C = 15 minute ceiling.

Ca = Potential occupational carcinogen. NIOSH recommends that occupational exposure be limited to the lowest 

 feasible concentration.
1. 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, National Institute for Occupational Safety and Health,

DHHS (NIOSH) Publication No. 92-100.

2. ACGIH [1995]. 1995-1996 threshold limit values for chemical substances and physical agents and

biological exposure indices. Cincinnati, OH: American Conference of Governmental Industrial

Hygienists.

3. Code of Federal Regulations [1993]. 29 CFR 1910 Washington, DC: U.S. Government Printing

Office, Federal Register.

4. Hernberg S, et al. [1988]. Lead and its compounds. In: Occupational medicine. 2nd ed. Chicago,

IL: Year Book Medical Publishers.

5. Landrigan PJ, et al. [1985]. Body lead burden: summary of epidemiological data on its relation to

environmental sources and toxic effects. In: Dietary and environmental lead: human health effects.

Amsterdam: Elsevier Science Publishers.

Figure 1. Photograph of steel grit inside an open 37mm cassette. This sample was collected by BIW during previous 

air monitoring.

 . 
6. Proctor NH, Hughes JP, Fischman ML [1991]. Lead. In: Chemical hazards of the workplace. 3rd

ed. Philadelphia, PA: J.B. Lippincott Company, Philadelphia, pp 353-357.

7. NIOSH [1978]. Occupational exposure to inorganic lead. Cincinnati, OH: U.S. Department of

Health, Education, and Welfare, Public Health Service, Centers for Disease Control, National

Institute for Occupational Safety and Health, DHEW (NIOSH) Publication No. 78-158.

8. Pirkle JL, et al. [1994]. The decline in blood lead levels in the United States, the National Health

and Nutrition Examination Surveys (NHANES). JAMA, 272:284-291.

9. DHHS [1990]. Healthy people 2000: national health promotion and disease objectives. Washington,

DC: U.S. Department of Health and Human Services, Public Health Service, DHHS Publication No.

(PHS) 91-50212.

10. ATSDR [1990]. Toxicological profile for lead. Atlanta, GA: U.S. Department of Health and

Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry. DHHS

(ATSDR) Publication No. TP-88/17.

11. Grandjean P and Bach E [1986]. Indirect exposures: the significance of bystanders at work and at

home. Am Ind Hyg Assoc J 47(12):819-824.

12. Farfel MR and Chisholm JJ [1990]. Health and environmental outcomes of traditional and modified

practices for abatement of residential lead-based paint. American Jour of Pub Health, 80:10, 1240-

1245.

13. EPA [1994]. Guidance on residential lead-based paint, lead-contaminated dust, and leadcontaminated soil. Washington, DC: U.S. Environmental Protection Agency, Office of Prevention,

Pesticides and Toxic Substances. Memorandum from Lynn Goldman, Assistant Administrator, July,

14, 1994.

14. CDC [1991]. Preventing lead poisoning in young children: a statement by the Centers for Disease

Control - October 1991. Atlanta, GA: U.S. Department of Health and Human Service, Public Health

Service, Centers for Disease Control.

15. Brody, DJ, et al. [1994]. Blood lead levels in the US population, phase 1 on the third National

Health and Nutrition Examination Survey (NHANES III, 1988 to 1991). JAMA 272: 277-283.

16. Webb M: Cadmium. Br Med Bull 1975;31:246-50.

17. Lauwerys R, Roels H, Regniers M, et al. Significance of cadmium concentration in blood and in

urine in workers exposed to cadmium. Environ Res 1979;20:375-91.

18. Kjellstrom T. Exposure and accumulation of cadmium in populations from Japan, the United States,

and Sweden. Environ Health Perspect 1979;28:169-97.

19. Ellis KJ, Vartsky D, Zanzi I, et al. Cadmium: in vivo measurement in smokers and nonsmokers.

Science 1979;205:323-25.

20. Friberg L, Piscator M, Nordberg GF, et al. Cadmium in the environment. Cleveland: CRC Press,

1974.
21. Baker EL, Peterson WA, Holtz J, Coleman C, Landrigan PJ. Subacute cadmium intoxication in

jewelry workers: an evaluation of diagnostic procedures. Arch Environ Health 1979;34:173-77.

22. Scott R, Paterson PJ, Mills EA, et al. Clinical and biochemical abnormalities in coppersmiths

exposed to cadmium. Lancet 1976;2:396-98.

23. Page LB, Culver PJ. A syllabus of laboratory examinations in clinical diagnosis. Cambridge:

Harvard University Press, 1962.

24. Rosen JF, Chesney R, Hamstra A, DeLuca H, Mahaffey K. Reduction in 1,25-dihydroxyvitamin D

in children with increased lead absorption. N Engl J Med 1980;302:1128-31.

25. Kazantzis G. Renal tubular dysfunction and abnormalities of calcium metabolism in cadmium

workers. Environ Health Perspect 1979;28:155-59.

26. Piscator M. Role of cadmium in carcinogenesis with special reference to cancer of the prostate.

Environ Health Perspect 1981;40:107-20.

27. Lemen RA, Lee JS, Wagoner JK, et al. Cancer mortality among cadmium production workers. Ann

NY Acad Sci 1976;271:273-79.

28. Thun MJ, Schnorr TM, Smith AB, Halperin WE, Lemen RA. Mortality among cadmium production

workers - an update. Journal of the Nat Cancer Inst 1985; 2:325-333.

29. Code of Federal Regulations [1993]. 29 CFR 1926 Washington, DC: U.S. Government Printing

Office, Federal Register.

30. Proctor NH, Hughes JP, Fischman ML [1988]. Chemical hazards of the workplace, 2nd ed.

Philadelphia, PA: J. B. Lippincott.

31. Blair A, Mason TJ [1980]. Cancer mortality in the United States counties with metal electroplating

industries. Arch Environ Health 35(2):92-94.

32. Franchini I, Magnani F, Mutti A [1983]. Mortality experience among chrome plating workers:

initial findings. Scand J Work Environ Health 9:247-252.

33. Royle H [1975]. Toxicity of chromic acid in the chromium plating industry. Environ Res 10:39-53.

34. Silverstein M, Mirer F, Kotelchuck D, Silverstein B, Bennett M [1981]. Mortality among workers

in a die-casting and electroplating plant. Scand J Work Environ Health 7 (suppl. 4):156-165.

35. Sorahan T, Burges DCL, Waterhouse JAH [1987]. A mortality study of nickel/chromium platers.

Br J Ind Med 44:250-258.