DOCUMENTS AND COMMITTEE REPORTS

Statistics Needed for

Determining the Effects of

the Environment on Health

Report of the Technical Consultant Panel

to the United States National Committee

on Vital and Health Statistics

Recommendations concerning which statistical data on health

effects of the environment should be collected, the ways in which

recommended data should be collected, and any changes that

should be made in the existing measurements of environmental

factors in order to relate the environmental factors to health effects

more efficiently.

DHEW Publication No. (PHS) 79-1457

Series 4

Number 20

U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE

Public Health Service

Off ice of Health Research, Statistics, and Technology

National Center for Health Statistics

Hyattsville, Md. July 1977
Vital and Health Statistics-Series4-No.20

First issued as DHEW Publication No. (HRA) 77-1457

July 1977
NATIONAL CENTER FOR HEALTH STATISTICS

DOROTHY P. RICE, Director

ROBERT A. ISRAEL, Deputy Director

JACOB J. FELDMAN, Ph.D., Associate .Directorfor Analysis

GAIL F. FISHER, Ph.D., Associate Director for the Cooperative Health Statistics System

ROBERT A. ISRAEL, Acting Associate Director for Data Systems

JAMES T. BAIRD, JR., Ph.D., Associate Director for International Statistics

ROBERT C. HUBER, Associate Director for Management

MONROE G. SIRKEN, Ph. D., Associate Director for Mathematical Statistics

PETER L. HURLEY, Associate Director for Operations

JAMES M. ROBEY, Ph.D., Associate D;rector for Program Development

PAUL E. LEAVERTON, Ph. D., Associate Director for Research

ALICE HAYWOOD, Information Officer

Library of Congress Cutalog tird Number 77-608058
FOREWORD

This report, prepared under the auspices of the U.S. National Committee on

Vital and Health Statistics, considers the needs for collecting statistics required in

determining the health effects of a broad variety of environmental conditions.

Although there is increasing public awtieness of the importance of the

environment on the health status of the U.S. population, there has been no

systematic national effort to assess the problems. To meet this urgent need, this

report was commissioned by the National Center for Health Statistics, the central

h~alth statistics collection unit for the Nation.

Kerr L. White, M.D.

Chairman

United States National Committee

on Vital and Health Statistics
U.S. NATIONAL COMMITTEE ON VITAL AND HEALTH STATISTICS

CHAIRMAN EXECUTIVE SECRETARY

Kerr L, White, M.D. James M. Robey, Ph.D.

Professor of Health Care Organization Associate Director for Program Development

School of Hygiene and Public Health National Center for Health Statistics

The Johns Hopkins University Health Resources Administration, PHS, DHEW

615 North Wolfe Street 3700 East-West Highway

Baltimore, Maryland 21205 Hyattsville, Md. 20782

MEMBERS

Mrs. Gwendolyn Johnson Acsadi

Chief, Fertility and Family Planning Studies

Section

Population Division

United Nations

New York, New York 10017

Alan D. Bauerschmidt, Ph.D.

Associate Professor of Management

College of Business Administration

University of South Carolina

Columbia, South Carolina 29208

Carol W. Buck, M.D., Ph.D.

Professor and Chairman

Department of Epidemiology and Preventive

Medicine

The University of Western Ontario

London, Ontario, Canada N6A 5B7

James P. Cooney, Jr., Ph.D.

Chief Executive Officer

Rhode Island Health Services Research, Inc.

56 Pine Street

Providence, Rhode Island 02903

.

Manning Feinleib, M.D.

Chief, Epidemiology Branch

National Heart and Lung Institute

National Institutes of Health, DHEW

Bethesda, Maryland 20014

Manuel A. Ferran, Ph.D.

President

El Vane State Bank

P. O. BOX 12186

Albuquerque, New Mexico 87102

Bernard G. Greenberg, Ph.D.

Dean

School of Public Health

University of North Carolina

Chapel Hill, North Carolina 27514

Marcus O. Kjelsberg, Ph.D.

Professor and Director

Division of Biometry

School of Public Health

University of Minnesota

1226 Mayo Memorial Building

Minneapolis, Minnesota 55455

Forest E. Ludden, Ed.D.

Director

Special Services Administration

State Department of Public Health

State Office Building

Montgomery, Alabama 36104

John D. Reid, Ph.D.

Chairman, Sociology Department

Atlanta University

233 Chestnut Street, S.W.

Atlanta, Georgia 30314
Mrs. Anne A. Scitovsky

Chief, Health Economics Division

Palo Alto Medical Research Foundation

860 Bryant Street

Palo Alto, California 94301

Ethel Shanas, Ph.D.

Professor of Sociology

College of Liberal Arts and Sciences

University of Illinois at Chicago Circle

BOX 4348

Chicago, Illinois 60680

Roger Hall Shannon, M.D.

President

Radiology Associates of Spokane

N. 5901 Lidgerwood

Spokane, Washington 99207

John E. “Wennberg, M.D.

Assistant Professor of Preventive and Social

Medicine

Harvard Medical School and

Member, Center for the Analysis of Health

Practices

Harvard School of Public Health

577 Huntington Avenue

Boston, Massachusetts 02115

CONSULTANTS AND STAFF

Consultants

Margaret Deane, MPH

Epidemiologist

Epidemiological Studies Laboratory

California State Department of Health

2151 Berkeley Way

Berkeley, California 94704

Pierre DeCoufle, SC.D.

Chief, Illness and Injury Surveillance Branch

National Institute for Occupational

Safety and Health, CDC, DHEW Park Building

Rockville, Maryland 20857

John R, Gold smith, M.D. (Chairman)

Medical Epidemiologist

Epidemiological Studies Laboratory

California State Department of Health

2151 Berkeley Way

Berkeley, California 947o4

John H. Knelson, M.D.

Acting Director

Health Effects Research Laboratory

U.S. Environmental Protection Agency

Research Triangle Park, N.C. 27711

Conrad P. Straub, Ph.D.

Professor and Director

Environmental Health

School of Public Health

University of Minnesota

1325 Mayo Memorial Building

Minneapolis, Minnesota 55455

Herman A. Tyroler, M.D.

Professor

School of Public Health

University of North Carolina

Chapel Hill, North Carolina 27514

James L. Whittenberger, M.D.

Professor of Physiology

James Stevens Simmons Professor

of Public Health

Harvard School of Public Health

665 Huntington Avenue

Boston, Massachusetts 02115

Staff

Esther Baginsky, A.B.

Public Health Statistician

Occupational Health Branch

California State Department of Health

2151 Berkeley Way

Berkeley, California 94704

v
William H. Clark, M.D.

Medical Officer

Public Health Division

California State Department of Health

2151 Berkeley Way

Berkeley, California 94704

Paul E. Leaverton, Ph.D. (NCHS Liaison)

Associate Director for Research

National Center for Health Statistics, HRA, PHS,

DHEW

HyattsviUe, Maryland 20782

Iwao M. Moriyama, Ph.Da

Chief, Epidemiology and Statistics Department

Radiation Effects Research Foundation

5-2 Hijiyama Park

Hiroshima, 730 Japan

William D. Simmons, M.P.H.

Regional Coordinator

Health Protection Division

California State Department of Health

2151 Berkeley Way

Berkeley, California 94704

April 8, 1974

July 11-12,1974

February 27-28, 1975

August 11-12, 1975

MEETINGS OF PANEL

Bethesda, Maryland November 18, 1975 Chicago, Illinois

Minneapolis, Minnesota Presentation and discussion at American

Washington, D.C.

Public Health Association Annual Meeting,

special session on Statistics, Environment,

Bethesda, Maryland and Occupational Health.

aFormerly Associate Director for International Statistics, National Center for Health Statistics.
CONTENTS

Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iii

U.S. National Committee on Vkal and Herdth Statistics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iv

ConsultantsandStaff . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . v

MeetingsofPanel . . . . . . . . ... ..0.. . . . . . . . . . . . . . . . . . , . . . . . . . . . . . . . . . . . . . . . . vi

Charge toConsultsnts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Findingsrmd Recommendations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Recommendations . . ;. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Types of Statistical Information and Analyses Considered by Panel of Consultants . . . . . . . . . . 5

Elaboration of Recommendations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

Recommendation I: National Death Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

Recommendation 2: Strengthened Epidemiolo@cCapability ofNCHS . . . . . . . . . . . . . . . 6

Recommendation :ProvisionofData byNCHS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

Recommendation 4: Use of Data From 1980 Census . . . . . . . . . . . . . . . . . . . . . . . . . . 7

Recommendation 5: Stan&rdizing Data Collection . . . . . . . . . . . . . . . . . . . . . . . . . . .

Recommendation 6: Data Collection by HIS and HES . . . . . . . . . . . . . . . . . . . . . . . . . ;

Recommendation 7: Morbidity and Place of Employment . . . . . . . . . . . . . . . . . . . . . . . 8

Recommendation 8: HSA’S and Environmental Health . . . . . . . . . . . . . . . . . . . . . . . . . 8

Major Environmental Contaminants Known or Swpetied To five Si@fimt Effe* on Hcakh . . . . 8

Types of Disease and Impairment to Which Environmental Contaminants Contribute . . . . . . . . . . . . 9

Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

Socioeconomic Status . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

Smoking . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

Diet and Alcohol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

Radiation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

Occupation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

Nonmalignant Respiratory Conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

CsrdiowiscukrC onditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

Carbon Monoxide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

Meteorological and Seasonal Influences.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

Water Hardness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

Social Environment . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

Industrird-Occupational Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

Developmental Abnormalities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

Pregnanc~Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

Teratog+ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

Somatic Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

Disease Related to Ingested Water Pollutants or Constituents . . . . . . . . . . . . . . . . . . . . . . . . 16

Waterborne Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16

Mutations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

Epidemiologic Methods Applicable to Environmental Health . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

Data Available for Analyses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

Group Comparisons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Community Exposure Versus Occupational Exposmes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ;

vii
Health Effects and Community Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Geographic Comparisons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Comparison sOverTime . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Temporo-S~tial Comparisons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Dose-Response Relationships . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Epidemiologic Monitonng and Surveillance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Effect of Interactive and Contributory Variables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Rare Events . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Health Effects and Occupationrd Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Existing Records . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Specird Ascertainment of Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Listof Detailed Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Appendixes .-

1.

n.

III.

Iv.

Occupational Disease Reportingin California . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ,.

Occupational Disease Reportingand Survey Results . . . . . . . . . . . . . . . . . . . . . . . . . . .

Mortality Surveillance Using Coroner’s Reports . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

‘fhe Continuous Work-History Sasnple . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

LIST OF FIGURES

1. Age-specific mortality for white males from emphysema, bronchitis, asthma, and obstructive lung

disease: United States, 1973 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

2. Average annual number of typhoid and hepatitis cases occurring in waterborne outbreaks1946-70 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

LIST OF TEXT TABLES

A. Mortality rates formspimto~ con&tions wsodated titientironmenti exposwes, bycolormd

sex: United States, 1968 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

B. Observed numbers of deaths andstandadizedm ortalityratios (SMR) forselected mcupational

groups exhibitirsg excess mortality frommalignant andnonmrd@ntrespiratorydiseasefor

males aged 20-64 years: United States, 1950 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

C. Average annual number of waterborne disease outbreaks, by type of system: United

States, 1938-70 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

D. Number of cases of waterborne disease per outbreak, by type of system: United

States, 1938-74 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

E. Number of outbreaks and cases of waterborne disease, by type of system and illness: United

States, 1961-70 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

20

20

20

21

21

21

21

22

22

22

22

23

26

36

39

41

45

13

17

11

12

16

16

17

...

Vlll
STATISTICS NEEDED FOR DETERMINING THE EFFECTS

OF THE ENVIRONMENT ON HEALTH

CHARGE TO CONSULTANTS

The past few decades have witnessed great

changes in the physical and chemical contaminants of the human environment and an increasing recognition of the impact of both the

physicaI and social environment on the health of

human, beings. Effects of environmental exposures cannot be isolated from effects of demographic factors and such habits as smoking.

Therefore, studies of the effects of these changes

in the environment on the health of the population have been inadequate to provide guidance

for policies affecting controI and protection.

The consultants on the TechnicaI Consultant

Panel to the U.S. National Committee on Vital

and Health Statistics will recommend which

statistical data on health effects of the environment should be collected, the ways in which

recommended data should be collected, and any

changes that should be made in the existing

measures of environmental factors in order to

relate better the environmental factors to the

health effects.

The consultants will consider the major

environmental contaminants known or suspected to significantly affect health, and will

specify the nature of the health effects and offer

evidence relevant to such statements. In doing

so, the panel should consider such problems as

low levels of exposure over long periods of time,

variation in population susceptibility, interaction and synergistic effects, delayed manifestations of effects over many years or even over

generations, the sequences of functional physiologic and pathologic response, and contrasts of

exposure due to population mobility.

The consultants will review, for such environment al factors. the kinds of data now

available on health effects, specify the data and

analyses needed to estimate the health effects,

and indicate the methods by which the data

cotdd be obtained in categories of methods such

as the foIIowing:

Analysis of routinely coIIected data on the

health of the population.

Special types of analysis which will aid in

detecting and monitoring health reactions.

Special surveys of occupational and other

exposed groups.

Disease registries in selected populations.

Monitoring of exposures and of health reactions.

Deficiencies of existing systems of measuring

exposure should also be noted.

Listed below are the types of conditions and

data that should be useful:

Relatively uncommon conditions with relatively high specificityy, e.g., mesothelioma in

relation to asbestos.

RelativeIy common conditions with poor

specificity —e.g., coronary heart disease in

relation to temperature, stress, or carbon

monoxide exposures.

Overall patterns of mortality and morbidity,

such as excess daily mortality, time of year

effects, urban-rural differences, and consequences of migration.

1
Because of the wide variety of environ- effects have been prepared, priorities should be

mental contaminants, the consultants may re- assigned in terms of the probable frequency and

strict their consideration to those with the more severity of the health effects in the population,

deleterious health effects. When recommenda- and the relevance of such data for control and

tions for collection of statistical data on health for prevention.

FINDINGS AND RECOMMENDATIONS

FINDINGS

Experience indicates that preventing those

environmental conditions that affect human

health is one of the most cost-effective strategies

for preventing disease and impairment.

A large but difficult to estimate portion of

the burden of such diseases as cancer and heart

disease can be attributed to environmental exposures.

Occupational exposures to specific materials,

because they are usually more intense and better

defined than community exposures, can indicate

agents that negatively affect health in the

community–causing disease and impairing

health or performance.

Identification of relationships between

health and environmental conditions requires

extensive epidemiological analysis of health and

environmental statistics as well as the collection

of new relevant data.

Potentially useful health statistics are available, but are not fully applied to environmental

problems. Among these are occupation and

industry statements recorded on death certificates, and data on industry and occupational

morbidity and mortality available from the

Social Security Administration, industrial organizations, and health care systems. Potentially

useful data concerning environmental exposure

are also available but are not fully linked to

health status information. Sources of such data

include the Environmental Protection Agency

(EPA), the National Institute of Occupational

Safety and Health (NIOSH), and the Food and

Drug Administration (FDA).

Local health planning activities, especially

those in health service agencies, need to evaluate

their environmental health programs and activities on the bases of health statistics as well as

on environmental exposure data.

RECOMMENDATIONS

The recommendations deal with several general topics, as follows:

The role and responsibility of the National

Center for Health Statistics (NCHS) in regard to environmental health statistics and

epidemiological studies of the environment

as it affects health.

The improvement and standardization of

statistical methods applicable to the study

and monitoring of environmental health.

The extension and broadening of NCHS’S

current survey procedures to include more

measures of environmental exposures.

The facilitation and performance of epidemiological studies using available data.

The establishment of new data systems

specifically designed to collect information

about environmental effects on health.

The following are the specific recommendations made by the panel:

1. Establish a national death index to permit determination of whether members

of a cohort of persons of known environmental exposure have died, and if dead,

where and when the death occurred.

2. Formally reco~ize the epidemiologic

responsibilities and substantially

strengthen the epidemiologic capability

at NCHS; some specific responsibilities

of such a protgramare

2.1 Plan and carry out epidemiologic

analyses of data obtained by the

Center or other agencies concerned

with the environment.

2
3.

2.2 Plan, conduct, and demonstrate the

usefulness of epidemiologic monitoring for prevention of unfavorable

health effects of existing environmental exposures. Such procedures

offer a possibility, as yet unproven,

for evaluating new materials and

technology whose health consequences are not otherwise known.

2.3 Facilitate and support the pooling

and interpretation of appropriate

data among all Federal, State, and

academic institutions concerned with

environment al health phenomena.

2.4 Provide increased opportunities for

epidemiologists to use NCHS data

for studies of the environment and

health.

2.5 Improve timeliness and accessibility

of the annual national mortality

summaries so that rates by time, area,

age, race, sex, and other factors may

be quickly and easily provided. This

also applies to the 10 percent national monthly sample of deaths and

will allow unusual patterns to be

noted quickly by epidemiologists.

Provision by the NCHS of data in such

format, detail, and timeliness that epidemiologic analysis can fecus on environmental health problems by such procedures as

3.1 Identification of excesses in mortality and morbidity in occupational

groups.

3.2 Analysis of variation in morbidity

and mortality by age, race, sex,

economic status, time of year, and

geo~aphic area in order to detect or

obtain evidence pointing toward environmental effects.

3.3 Detection of disease or impairment

gradients which may be related to

community air quality, including

sulfur oxides and particulate matter,

photochemical oxidants, and pollutants emitted from mines, mills, or

smelters.

3.4 Analysis of daily mortality in relation to environmental factors

4.

5.

e

within and between selected metropolitan areas.

3.5 Detection of disease or impairment

which may be related to water quality including the presence of organic

compounds, “hardness,” heavy

metals, and viral and other microbizd

agents.

3.6 Early identification of rare types of

mortality and morbidity associated

with environmental exposures.

3.7 Identification, in association with

occupational exposures, of disease or

impairment which may also be occurring as a result of community

exposure.

Obtain data from the 1980 census on

occupational and environment al exposures with the following objectives:

.4.1 To obtain occupational mortality

rates by cause, adjusted (or specific)

by age, race, and sex.

4.2 To obtain income, education, or

other socioeconomic gradients by

cause, adjusted (or specific) by age,

race, and sex.

4.3 To obtain differential mortzdity rates

by cause in locations with contrasting levels of air or water pollution or of urbanization, using age,

race, sex-adjusted (or specific) data.

4.4 To obtain by means of census or

health survey procedures, data on

differences by location in cigarette

smoking, alcohol and drug use, and

in dietary composition and motor

vehicle use, comparable in time and

location to data obtained in items

4.1-4.3 asjust listed.

4.5 To obtain, at least on a pilot basis,

data on usual occupation and duration of residence in a given community from the 1980 census for comparison with death certificate data.

Develop and standardize statistical and

data collection procedures relevant to

environmental exposures for application

to mortality data, data from the U.S.

Bureau of the Census, and data collected

by other government agencies. These

3
should be designed to permit comparisons with information from other countries, such as that from the United

Kingdom-Registrar General’s decennial

report.l

This effort will require a review of codes

and coding procedures, particularly with

respect to occupation, housing, and migration, for both the Center and the

1980 U.S. census.

6. Establish as ongoing activities of NCHS’S

Health Interview Survey (HIS) and

Health Examination Survey (HES) the

collection of data on environmental exposures and morbidity or other environmentally relevant effects including, but

not limited to:

6.1 Collection of water, food, or other

sampIes which reflect environmental

exposures in individual households.

6.2 Sampling of human tissues or excreta

to measure exposure to pollutants.

Measurements must be based on population samples from which results

can be extrapolated to defined populations. For pollutants that are

stable in the body, estimation of the

body burden offers several advantages over estimation of exposure

based on analysis of environmental

samples; these advantages include the

ability to estimate the effects of

multiple routes of exposure, more

valid estimation of dose, and the

opportunity to observe fluctuations

in body burden and to detect active

metabolizes.

6.3 Analysis of data on physiological,

biochemical, or psychological reactions which may be related to environmental exposures.

7. Increase efforts to determine what proportion of morbidity is due to conditions at the place of employment. The

experience in the California Health Department and the survey results in

Oregon and Washin~on published by

NIOSHZ provide examples of practical

and valid methods. The objectives would

include

7.1 Estimation of the extent and kinds

of occupational disease as a means

for its prevention and for equitable

attribution of its costs.

7.2 Delineation of problem areas reflecting possible inadequacies of health

standards.

7.3 Provision of information from pilot

studies and from the Health Interview Survey to be used in studies of

the prevention of occupational disease.

7.4 Initiation of studies of long-term

effects of carcinogenic, mutagenic,

and teratogenic agents in the workplace.

8. Local health planning agencies should

use mortality statistics and hospital admission and discharge data, as well as

special surveys, to determine the amount

and type of environmentally related disease present in their locality, and trends

thereof. This should include

8.1 Use of comparative mortality data

by county. Such data are already

published by site for cancers and are

to be pubIished for other diseases.

8.2 Identification of environmental components and the use of this information for local health planning for the

following diseases: cancer of urinary

and respiratory tract, skin cancer,

lymphoma and leukemia, bronchitis,

asthma, emphysema, and other respiratory conditions. In interpreting

data, the interaction between environmental exposures and smoking

must be considered.

8.3 Support by health service agencies

on the development of local data on

occupational injury and disease in

relation to industrial employment

and pollutant exposures.

8.4 Epidemiologic monitoring based on

such data to help evaluate local

achievements in environmental

health.
TYPES OF STATISTICAL INFORMATION

AND ANALYSES CONSIDERED BY

PANEL OF CONSULTANTS

The panel first considered routineIy collected vital statistics, many of which are directly

applicable to determining the health effects of

environmental exposure since many specific

causes of death imply a relevant environmental

exposure. Included among these causes of death

are the specific occupationally related conditions such as pneumoconioses and the specific

intoxications and accidents that are related to

environmental conditions.

Furthermore, many deaths and illnesses are

related to environmental exposures, for example, those due to cancer, heart disease, and

respiratory conditions. The proportion of cancer

by site attributable to occupation and other

environmental conditions according to “sound

ctiological hypotheses” is discussed in more

detail later in this report (see subsection

“Cancer” under “Types of Disease and Impairment to Which Environmental Contaminants

Contribute”). The tabulation presented there

based on an analysis by Higginson and Muir4 of

the International Agency for Research on

Cancer, reflects worldwide data and may represent a substantial understatement of the loca.I

effects of environmental conditions. Higginson

has also said that, compared to the lowest cancer

experience in a developed country, most other

areas show an excess which suggests that 80

percent of cancer has an environmental origin.

It is necessary that other data not now

included in the vital statistics system be utilized

in looking for effects of environmental exposures. These include data on morta.Iity among

social security recipients and data on disability

among social security groups. These data can be

classified by industry, location, and in the case

of disability, by occupation and cause of dkability. Other sources of data include the information available through cancer registries and

through registries of other specific diseases or

agents, data obtained from various pension and

insurance systems, data obtained from the

Veterans Administration and from the military,

and morbidky data obtained from school health

and occupational health programs.

Potentially useful data, but in need of

evaluation are

Reports obtained in coroners’ offices from

Iarge cities that might reflect short-term

fluctuations in mortality associated with

environmental changes. (See appendix III.)

Data on the occurrence of occupational

injury and occupational disease. These may

be useful in epidemiologic monitoring. (See

also appendixes I and II.)

The panel next considered the need for more

adequate epidemiologic analysis of data which

are available from various sources. Such analysis

might detect differences among States, counties,

or communities within a large metropolitan area

in order to determine whether there are “hot

spots” in one or more locations that would

offer leads for a possible environmental cause.

Such data have been analyzed with respect to

cancer by a group at the National Cancer

Institutes ~6 and the implications are now being

assessed by that Institute, the Environmental

Protection Agency, and others. In addition, the

intensive long-term study of statement of occupation recorded on death certificates in the

State of Washington provides a useful form of

analysis.7 The decennial reports of the Registrar

General’s Office in Great Britainl suggests additional analyses which should be considered in

the United States. The objective of this type of

analysis is to define the need for environmental

exposure information applicable to environmental control measures to reduce exposures as

well as the need for conducting prospective and

retrospective epidemiologic studies.

The third major type of work considered by

the panel involves the collection and interpretation of new data in which both environmental

exposure and health reactions are obtained for

defined populations or population cohorts.

These represent a more active application of

epidemiologic skills and staff to the problems of

determining health effects associated with environmental conditions. The panel strongly recommends that such work be systematically

undertaken using a variety of sources of health

statistical information.

5
ELABORATION OF RECOMMENDATIONS

Recommendation 1:

National Death Index

Recommendation 1 supports a national

death index. This would provide information on

whether or not a given person has died in a

specified year in which death-registration area.

Such a registry would be of invaluable assistance

to environmental and other epidemiologists.

Recommendation 2:

Strengthened Epidemiologic

Capability of N(2HS

The use of health statistics to determine the

health effects of environmental conditions is

fundamentally an epidemiologic problem, and

yet there is no epidemiologic unit in the

National Center for Health Statistics. The responsibilities of such a unit need not be Iimited

to environmental health problems. Accordingly,

the panel recommends that such a unit be

established and that it be charged to carry out

the epidemiologic analysis not only of data

obtained in the Center but also of data available

through other components of the Department of

Health, Education, and Welfare, such as the

Social Security Administration, and through

other branches of government and of industry.

Responsibility for such a program isauthorized by

the Federal legislation empowering the Center

and the U.S. National Committee on Vital and

Health Statistics to colIect and analyze statistics

on the determinants of heahh.

In addition NCHS should take an active role

in bringing together the various organizations

and agencies which can provide relevant data on

a national or local basis and promote the use of

comparable geographic and population bases for

data on environmental exposures. Such efforts

have been greatly needed and it is a natural

function for the Center to carry them out.

There should be a provision for epidemiologic

studies and monitoring to be carried out within

the Federal Government by persons on short- or

medium-term assignment. Such assignments

could come from personneI in other Federal

agencies, from State or local governments

through the Intergovernmental Personnel Exchange Act of 1971, or from international

assignments. Thus, we recommend that the

epidemiologic unit provide opportunities for

epidemiologists to work on any aspect of the

Federal health statistical system, and we further

recommend that the unit provide service for

epidemiologists who are working elsewhere on

environmental problems.

Recommendation 3:

Provision of Data by NCHS

The charge to the panel provides guidelines

to specify the sorts of data which are likely to

indicate environmental contributions.

The certificate of death generally includes

information on occupation, but such information is not being systematically utilized. The

experience in the States of California and

Washington and in Great Britain demonstrates

that occupational analysis is worthwhile and the

panel recommends (recommendation 3.1) that

such ardyses be made available. At the panel’s

request, the staff of NCHS prepared a review of

a O.167-percent systematic sample of the death

records for 1 year and found that there were

usable occupational statements in 90 percent of

male deaths in the age group 20-44, 86 percent

in the age group 45-64, and 73 percent in those

65 and over.

The variation in morbidity and mortality by

time and by location indicates the likelihood,

but does not prove the existence of, an environmental effect. It is therefore important to detect

unfavorable locations and trends to see whether

there are associated environmental changes. This

effort might be incorporated into a more active

epidemiolo~c monitoring program (recommendation 3.2),

There is no doubt that community air

pollution exposures can result in aggravation of

bronchitis, emphysema, and asthma. Morbidity

and mortality from these diseases also are

strongly associated with cigarette smoking. An

excess of mortality from these causes has been

reported in urban areas, but morbidity data

from the National Health Interview Survey fail

to show an urban excess. These data have not

been analyzed with regard to probable air

pollution exposure. This should be undertaken

{recommendation 3.3). These analyses should

6
include fluctuations in daily mortality (recommendation 3.4). Experience has been that analysis of daily mortality requires a population base

of about a million persons. (See “Daily Mortality Data” in appendix III.)

A pilot study is presently being supported in

the National Health Examination Survey to

determine the possible role of water hardness in

relation to cardiovascular disease. The panel

believes that studies relating water constituents

to disease have been undersupported and should

be augmented (recommendation 3.5).

The recent detection of angiosarcoma of the

liver in persons exposed to vinylchloride has

focused attention on the need for detecting rare

types of disease that may specifically relate to

certain types of exposure. A similar situation occurred with the relationship of mesothelioma to

exposures to asbestos, either in the workplace or

in the community. Nevertheless, the present vital

statistics system is not efficient in detecting rare

disease that have a peculiar clustering or that

have a substantial increase. It is necessary, therefore, to evaluate the sensitivity of the health statistics system with respect to detecting uncommon diseases and causes of death (recommendation 3.6).

Recent studies of cancer by area show that

high lung cancer rates occur in both men and

women in counties with nonferrous metal

smelters—evidence of communitywide effects of

industrial pollutants.c Other examples occur

with respect to lead, cadmium, and asbestos.

Thus industrial health effects may imply possibly communitywide effects and should be

evaluated (recommendation 3.7).

Recommendation 4:

Use of Data From 1980 Census

The British Registrar General’s Office has

analyzed occupational-social class gradients in

mortality every 10 years, not only for men but

also for women by their husbands’ occupation

and social class. We believe that the United

States has been remiss in not performing simikustudies. We recommend that a carefully planned

occupational and environmental analysis be

done for the next 3-year pericensal period

(1979-81). The guidelines for such studies could

be developed following the review of the analysis of occupation done in this country in 1950,8

and by reference to the most recent report of

the British Registrar General’s Office,l which

dealt with the 1961 British census data. We

believe that this should represent an international collaborative effort, but that the plans

should include studies on drug use, smoking, and

alcohol use, as well as studies involving environmental exposure estimations. In preparation for

this effort, it is necessary to review the classification, coding, and tabulation procedures currently in use to ensure that they are suitable for

comparative studies over time within the United

States as well asbetween different countries.

Recommendation 5:

Standardizing Data Collection

Comparability between census and vital statistics procedures has been a problem in many

studies of environmental factors and their influence on health. A common and wellstandardized set of procedures for obtaining,

recording, and coding occupation, industry, and

materials to which people are exposed can

increase such comparability and improve the

cost-effectiveness of the collection of health

data and environmental exposure data.

The work will involve development of compatible information and coding practices with, at

least, the Census Bureau, dealing with housing

and migration as well as industry, occupation,

and migration. (See also “Health Effects and

Occupational Exposures” near end of text.)

Standardization to tobacco smoking histories

would also be desirable. The work could be done

by task groups and should be pretested early

enough to be used in the 1980 census. The

experience of NCHS with coding and tabulating

data on illness, disability, and death will serve to

further standardize these other variables.

Recommendation 6:

Data Collection by HIS and HES

The National Center for Health Statistics has

not used the Health Interview Survey and Health

Examination Survey with maximum effectiveness to relate environmental exposures and their

effects. The panel, therefore, believes that there

7
should be systematic effort to obtain relevant

data to establish a more adequate monitoring of

environmental health effects. Such an activity

could extend to the collection of data on water

use and water quality as supplied in the household, food consumption practices, the use of

household agents such as pesticides, and materials that present an accident hazard, such as

firearms or flammables.

In addition, the Health Examination Survey

could be used for the collection of physiologic,

biochemical, and psychological information that

may be relevant to environmental exposures.

The surveys have been a major source of data on

smoking practices, but the data need to be

supplemented so that population distributions

of smoking can be obtained by State and by

occupation and socioeconomic status. The increased sample size necessary for this purpose

can easily be justified.

Sampling principles must be established for

estimating exposure to pollutants within large

and defined population groups. Although some

work of this sort has already been done by the

EPA, a coordinated program is needed and the

involvement of the Center in interpreting the

studies is important. Such measurements will

add a physiochemical dimension to evaluation

of exposure and may provide early evidence of

possible dkease or impairment.

Recommendation 7:

Morbidity and Place of Employment

No national occupational morbidity reporting system exists in the United States. Ongoing

programs in the State of California have been

only marginally supported (see appendix I).

Nevertheless, they have yielded much information of value for the early detection of occupational hazards.g Some data are also compiled by

the Bureau of Labor Statistics of the Department of Labor. The recent pilot study in the

States of Oregon and Washington indicates that a

high proportion of chronic conditions among

working-age adults may be related to conditions

of employ ment.z A systematic effort is needed

to extend these programs and to define the true

dimensions of the environmental burden of

disease and impairment. Such a program can

provide early clues for predicting community

hazards and thus help prevent them. The

strengthened occupational disease reporting system should be funded for limited followup

studies and for an ongoing monitoring operation

that reflects the major types of industrial and

occupational hazards in the country. 10

Recommendation 8:

HSA’S and Environmental Health

Local health service agencies (HSA’S) should

consider environmental health problems and

activities. Some guidelines are proposed in recommendation 8. The National Center provides

data on mortality by county, but additional

effort will be required to comply with Federal

Regulation 122.107 (c) (Federal Register 41

#60 p. 12828, March 26, 1976) which states in

part that: “The agency shall assemble and

analyze data concerning. . . the envir~nmental

and occupational exposure factors affecting

immediate and long term heahh conditions. ”

The purpose of this report as a whole is to

facilitate compliance with this requirement, but

from time to time data on dkeases and environmental exposures conditions should be compiled, reviewed, and discussed. The role environmental factors play in cancer, heart disease, and

developmental abnormalities is presented later in

the report as a means of supporting activities

that abet compliance with the Federal regulation

(see “Types of Disease and Impairment to which

Environmental Contaminants Contribute.”)

MAJOR ENVIRONMENTAL CONTAMINANTS KNOWN

OR SUSPECTED TO HAVE SIGNIFICANT EFFECTS ON HEALTH

A considerable number of environmental shown in table 1; the effects are classified as

agents are thought to affect human health “definite” or “possible.” “Appropriate circumsignificantly given appropriate circumstances. stances” may consist of characteristics of the

These agents, and their related effects, are exposed population, such as preexisting disease;

8
characteristics of the agent, such as concentration; or other characteristics of the specific

exposure, such as the presence of other agents.

By no means does each exposure produce the

effects described, nor have some of the “possible” effects been definitely established. Furthermore, no attempt has been made to quantify

the relationships. Further information about the

effects of the specific agents described can be

found in the World Health Organization monograph “Health Hazards of the Human Environment.”1 1

Quantitative estimates for many of the more

important effects have been established by

documents designated as criteria reports. Air

quality criteria reports for community exposures

are available for such pollutants as sulfur oxides,l Z particulate matter,l 3 ozone,l 4 carbon

monoxide,1 5 nitrogen dioxide,l G and hydrocarbons.1 T Some examples of the air quality

standards based on the criteria described in these

reports are given in table 2.18 Criteria reports

for occupational exposures are being prepared

by consultants to the National Institute for

Occupational Safety and Health (NIOSH). Dates

of completion of criteria reportsl 9 for some of

the substances are given in table 3.

Estimates of the numbers of persons at risk

because of occupational exposure to certain

agents are also shown in table 3. These were

prepared by NIOSH, which has also established a

“severity rating” of the health effects based on

the judgment of a panel. These evaluations of

the health impact of the agents are used to

determine priorities for preparing and issuing

criteria documents and for conducting research.

TYPES OF DISEASE AND IMPAIRMENT TO WHICH

ENVIRONMENTAL CONTAMINANTS CONTRIBUTE

Selected disease categories on which environmental exposures have an impact are the subject

considered now. Not all diseases and organ

systems afflicted by environmental contaminants are included here, and their omission

should not be interpreted as implying no environmental effect. -

CANCER

A table showing estimates

cancers at selected sites for

-of the percent of

which there are

“sound etiological hypotheses” was published in

1973 by Higginson and Muir4 (table 4). In view

of reports since 1973, these estimates should be

considered conservative.

Proportions of cancer attributed to occupational or other environmental factors will be

higher among adult males than in the total

population because a higher proportion of males

are employed in industry. In addition, the

overall age-adjusted incidence rate (excluding

nonmelanotic skin cancer) for males is higher,

estimated at 346.8 per 100,000 in the Third

National Cancer Surveyz 0 compared with 270.2

for females.

For more than half the cancers observed in

the Third National Cancer Survey, an external

causative agent is suspected on the basis of

“sound e~iological hypotheses,” About 5 percent

of all cancers are believed to be related to

occupation. Since occupational exposure to carcinogens occurs mainly in males, the implication

is that about 10 percent of male cancers are

related to occupation. These are conservative

estimates based on available direct evidence. In

addition, indirect evidence from population migration data suggests that environmental factors

are not yet identified for cancer of stomach, ●

colon, rectum, lung, and breast. Geographic

variation is marked for cancer of the cervix,

liver, bladder, and esophagus ;Z1 and environmental factors are being sought for these sites as

well.

in its publication “Cancer Rates and

Risksy’zz the National Cancer Institute has

shown that the occurrence of cancer varies with

socioeconomic status, cigarette smoking, diet,

alcohol, radiation, and occupation.

Socioeconomic Status

The association with low socioeconomic

status is generally quite marked for cancer of the

9
I

cervix, esophagus, and stomach, but smaller and

in the opposite direction for cancer of the

female breast. The lowest socioeconomic group

has the highest incidence for cancers of the

buccal cavity and respiratory system.

The relationships between cancer risk and

socioeconomic status are not fully understood,

but differences in general way of life, quality of

medical care, and degree of exposure to carcinogenic materials in the environment may be

contributing factors.

Smoking

No one now seriously disputes that lung

cancer deaths occur much more frequently

among cigarette smokers than among nonsmokers, and recent research has been directed

toward elucidating the meaning of this correlation.z 3 Epidemiologic studies show that cigarette smokers as well as pipe and cigar smokers

have a significantly higher risk of developing

laryngeal cancer than nonsmokers do, and that

smoking contributes to the development of

cancer of the oral cavity, esophagus, and lip. A

significant association has also been shown

between cigarette smoking and cancer of the

urinary bladder.

Certain occupational exposures have been

found to be associated with an increased risk of

dying from lung cancer. Cigarette smoking appears to interact with some of these exposures

to produce much higher lung cancer death rates

than those which occur among nonsmokers with

similar occupational exposures.

Diet and Alcohol

Observations on human populations have so

far uncovered relatively few forms of cancer that

can be linked with food intake.z 4 The high

incidence of cancer of the oropharynx and

esophagus among residents of the far north of

Sweden and Finland may be related to multiple

dietary deficiencies. Iodine deficiency may be

related to development of cancer of the thyroid.

Undernourishment or malnourishment can contribute to the high frequency of cirrhosis of the

liver and the later appearance of liver cancer

among some groups of African Negroes, Chinese,

Japanese, and others. Aflatoxin, a liver carcinogen, has been identified as a contaminant of

nuts and other foodstuffs in areas of high liver

cancer incidence.

Geographic differences have suggested a relationship between the highly refined Western diet

rich in starches and deficient in bulk with the

elevated risks for bowel cancer in North America

and Western Europe.

Cancers of the stomach and large bowel

among the Japanese in Hawaii are being studied

using migrant groups who experienced different

lengths of exposure to their countries of origin.

From studies of Japanese migrant groups, stomach cancer has been associated with consumption of foods preserved or pickled in salt; large

bowel cancer has been similarly associated with

the consumption of beef. The study of

Scandinavian immigrants to the United States25

has led to a suggestion that inadequate intake of

fruit and vegetables could be related to high

stomach cancer rates.

The association between excessive alcohol

consumption and cancers of the buccal cavity,

pharynx, larynx, and esophagus is now well

established.

Radiation

There is cIear evidence that radiation can

cause cancer in human beings.z 6 Although at

present the number of tumors induced by

artificial radiation constitutes only a very tiny

fraction of all human cancer, the hazard potential will increase because of increasing use of

radioactive substances in industry and medicine.

Only monitoring and control activities can minimize this hazard.

Further investigations are needed to measure

with greater precision the frequency of

radiation-induced malignancies and to determine

the relation between radiation dose, latent period, and cancer incidence rates.

Occupation

Even before the advent of the modem

industrial era, an association between occupation and the occurrence of cancer was recog

nized. However, immense growth of modem

industry has brought with it an increasing

number and diversity of carcinogenic substances,

10
many of which are associated with particular

occupations or industries. Some of the known

occupational cancers are listed in table 5.2z

Mortality statistics of broad occupational

groups provide additional leads (table 6).2 2

More detailed tables show that miners, laborers,

and transportation workers have an increased

risk of cancer, and that men in agricultural

pursuits (nearIy aII of whom live in rural areas)

have comparatively low mortality rates for all

cancer sites except skin.8 These findings are

confirmed by similar data collected in England

and Wales.1

The combination of a long latent period

between exposure and the development of

cancer, changes in exposure with time, incomplete diagnosis of some types of tumor, errors in

reporting occupation in censuses and on death

certificates, effects attributable to nonoccupational agents, and other factors make it difficult

to detect small increases in cancer risk in specific

occupation groups.

NONMALIGNANT RESPIRATORY

CONDITIONS

Most of the same environmental exposures

that contribute to excess rates of respiratory

cancer also contribute to elevated rates of

morbidity and mortality for bronchitis and

pulmonary emphysema and, to a lesser extent,

asthma. These three conditions, often collectively designated as “chronic obstructive pulmonary disease,” are found much more frequently

among smokers than among nonsmokers,z 3 have

higher mortality among low income urban populations compared with upper income or rural

residents, and show a predilection for individuals

working in certain occupations.T Fatal asthma is

twice as common among other races as among

the white race. Fatal tuberculosis is three times

as common. Emphysema and Iung cancer are

five times as common in males as in females.

While the prevalence and incidence of chronic

interstitial pneumonia is more than three times

that of active tuberculosis, the fatality rate is

substantially less. Some of these patterns are

shown in the morbidity data in tables 7 and 8

and in the mortality data in table A.zTY28

Mortality data by occupation for both malignant and nonmalignant chronic respiratory disease are shown for certain occupational groups

in table B.8 Some parallelism is noted between

malignant and nonmalignant respiratory diseases

with respect to occupational distribution. For

certain occupations, mortality is increased both

for malignant and nonmalignant respiratory disease in men aged 20-64.

Six prospective studies and one retrospective

study of the relative contribution that smoking

makes to mortality from chronic obstructive

bronchopulmonary disease permits the inference

that approximately 90 percent of chronic obstructive pulmonary disease is associated with

cigarette smoking.z 3 A further contribution is

made by variables associated with economic

status and exposure to poIlution.

Table A. Mortality rates for respiratory conditions associated with environmental exposures, by color and sex: United States, 1968

I

Total II White I Other

Condition

Both Male Fe- Male Fe- Male Fesexes male male male

Rate per 100,000

Chronic bronchitis . . . . . ... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.7 4.3 1.2 4.6 1.3 ;.: 0.5

Emphysema . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12.1 20.9 3.7 22.6 4.0 1.5

Asthma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.3 1.3 1.4 1.1 1.2 2:B 2.8

Pneumoconiosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0.8 1.6 0 1.8 0 0.5 0

Chronic interstitial pneumonia.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.7 2.3 1.2 2.4 1.2 1.7 0.7

Malignant disease ofrespiratory system. . . . . . . . . . . . . . . . . . . . . . . . . . . 31.8 53.5 11.1 54.7 11.4 44.3 8.4

SOURCE: National Center for Health Statistics: Vital Statistics of the United States, 1968, Vol. H, Part A. DHEW Pub. No. (HSM)

72-1101. Health Services and Mental Health Administration, Washington. U.S. Government Printing Office, 1972.

11
Table B shows

occupations. Since

selected examples of such

bronchitis and asthma are

ofte~ associated with environmental exposure,

but are at least potentially reversible, they

provide a warning of the possibility of other

diseases related to such exposures and thus point

the way to preventing later irreversible effects

such as lung cancer. On the other hand, both

groups of diseases are strongly associated with

cigarette smoking, and such occupations may

include a large proportion of smokers. The data

shown in table B are more than 25 years old and

may be reflecting occupational exposures occurring considerably farther back. Recent data

are badly needed for study of the relationship

between occupation and chronic disease of the

lungs and other organs.

Overall mortality from chronic lung diseases

has risen sharply during the period since 1950,

probably reflecting the interaction of smoking,

occupational changes, and increased air pollution. Since 1968, however, this rate has leveled

off .

These trends are difficult to interpret since

1968 because of the increase in certification to

“chronic obstructive lung” (or pulmonary) disease. These certifications are assumed to represent deaths that previously had been coded to

emphysema with bronchitis, or bronchitis with

emphysema. A new code, 519.3, was finally

introduced in 1971, but even when cleaths

attributed to this code are added to emphysema

mortality, the rates are not increasing as much as

they did prior to 1968. Deaths allocated to this

code combined with deaths allocated to the

codes for emphysema and chronic bronchitis are

shown in figure 1. Although overall mortality is

still increasing from this group, between 1969

and 1973 the high rates for persons aged 65-85

years are accompanied by a decrease in the

age-specific rates for men under 55. The change

in pattern of mortality from chronic conditions

among young people may be predictive of what

will occur on a larger scale among the whole

population. For example, the decrease in mortality from chronic nonmalignant respiratory diseases among young men may reflect a decreased

influence of cigarette smoking and possibly a

change in working conditions. A similar decrease

in lung cancer mortality in young men in Great

Britain has now extended to older men.z g

Among women, however, the upward trend

continues at all ages, zdthough the rates are not

as high. Women have increased their use of

Table B. Observed numbers of deaths and standardized mortality ratios (SMR) for selected occupational groups exhibiting excess

mortality from malignant and nonmalignant respiratory diseasefor males aged 20-64 years: United States, 1950

Occupational group

Mortal ity from Nonmalignant malignant neoplesms of respiratory

trachea, diseaseother

bronchus, and than influenza

lung and pneumonia

I Deaths SMR Deaths SMR

*

Barbars, etc, . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Cooks, except private household., . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Machinists andjobsetters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Molders, matal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Painters (construction), paperhange~, and glaziers . . . . . . . . . . . . , . . . . . . . . . . ., . . . . . . .

Taxicab drivers and chauffeurs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Laborere, woodproducts, etc.... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Laborers, primary metal industries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Laborers, transportation equipment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Operatives, etc., primary metal industrial . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

95

91

190

34

212

77

414

82

30

77

1151

1165

1138

1227

1167

1188

1138

1167

1200

1145

29

41

66

30

64

36

20

49

26

41

126

1195

125

1500

2133

1225

l;=

1433

1195

lSMR significantly above 100 at p <.01.

2SMR significantly above 100 at P ~ .05.

SOURCE: National Office of Vitsd Statistics: Mortality by occupation and cause of death among men 20-64 years of age: United

States, 1950, by L. Guralnick. Vital Statistics-Special Reports, Vol. 53, No. 3. Public Health Service. Washington, D. C., Sept. 1963.

12
— 1969

,/

..-”-

. . . . . . . ..- 1973 ,/

t’

/“

/[

/’

/’

/

Percent

Age change

/’

group per year

/’

35.44 -7.5

45.54 -1.9

/’ 55.64 +0.4

‘65.74 +2,4

/

75.84 +.7.7

85+ +8. 1

1~

85 years

years years years years years and over

AGE GROUP

Figure 1. Age-specific mortality for white males from eMDhVsema, bronchitis, asthma, and obstructive lung disease:

United States, 1969 and 1973

cigarettes in many age groups, but the proportion of men who smoke has declined in every

age group.30

CARDIOVASCULAR CONDITIONS

The epidemiologic understanding of the

determinants of adult-acquired, noninfectious

heart disease, particularly coronary heart disease

(CHD), is probably as advanced as that for any

chronic disease. The list of identified personal

risk factors is long and includes personal habits

such as diet and cigarette smoking that interact

with the environment, as well as blood pressure,

serum cholesterol, blood glucose, uric acid, body

mass, sedentariness, and personality type. In

spite of successes in understanding and predicting CHD in populations, no more than

perhaps 50 percent of cases are expkiined by the

established risk factors.s 1

Carbon Monoxide

There is convincing clinical experimental

evidence that exposure to carbon monoxide

(CO) and raised carboxyhemoglobin (COHb)

levels exacerbate symptoms of angina, and there

is laboratory evidence of myocardial ischemia

with reduced exercise tolerance.32 Increased

case fatality rates associated with increased

COHb suggest that the prognosis of acute myocardial infarct is affected by exposure to CO.

Some laboratory evidence implicates chronic CO

exposure as a possible atherogenic agent. This

has yet to be demonstrated in man by epidemiologic evidence.

Meteorological and Seasonal Influences

Strong statistical associations exist between

season, yearly temperature changes, and mortality attributed to CHD. In temperate climates,

deaths increase in winter and decrease in

summer. No doubt infectious agents are a

contributor. Coincident changes have been reported in serum cholesterol. Whether this is a

direct effect of temperature or secondary to

changes in diet, exercise, or other environmental

factors is not clear. Increases occur in daily

mortality in association with marked changes in

temperature and humidity.s 3

Water Hardness

There is a large and controversial literature

on the inverse relationship between water hardness and cardiovascular disease (CVD).34 Recent

reviews have given attention to:

Statistical associations.

Possible mechanisms by which trace metals

may cause increased susceptibility to sudden

deaths from arrythmia.

NaturaI experiments, i.e., the experience of

selected geographic areas with respect to

CVD mortality before and after changing

water quality.

Social Environment

A large body of evidence suggests that the

transition of a society from rural, agmrian to an

13
urbanized, industrialized economy is accompanied by a rise in CHD. We do not know how

much of this can be attributed to increases in

the risk factors just identified, how much to

changes in personal habits, how much to social

and psychologic stress, and how much to unidentified agents in the physiochemical environment.

Industrial-Occupational Agents

One industrial agent, carbon disulfide (CS2 ),

is associated with CHD in epidemiologic studies.

There is also some supporting clinical and

Laboratory evidence suggesting a mode of action

through production of hypercholesterolemia.

The evidence is far from conclusive or even

convincing; however, it does suggest a systematic

search for occupational groups with experience

analagous to that of viscose rayon workers’

excess of CHD and exposure to CS2.

One additional agent, freon, is a possible

provocatant of arrhythmia in occupationally

exposed pathologists and in laboratory animals.

DEVELOPMENTAL ABNORMALITY ES

Pregnancy Outcome

We are presently limited in our ability to

describe or understand possible effects of a

multitude of chemicals and other environmental

factors, either independently or through interactions, on the outcome of human pregnancies.

However, inability to perceive ill effects gives no

assurance that they are not occurring. Several of

the reproductive processes are known to be

affected by exposure to toxic substances.

The maternal organism.–During pregnancy

the maternal organism is more vulnerable.

Detoxification mechanisms are altered and

changes in protein, carbohydrate, and lipid

metabolism occur which may affect the impact

of environmental agents on pre~ancy duration

and outcome. We do not know what initiates

spontaneous labor but we do recognize a group

of substances that can stimulate or retard the

progress of labor, and it is conceivable that

substances with similar action might exist among

the large number of chemicals in the environment.

Embryonic development.–The developing

product of conception within the first 8 weeks

has a high and variabIe susceptibility to environmental influences. This is the time when a great

majority of teratoIogical effects are induced and

the conditions of exposure and types of agents

are of particular concern in relation to structural

defects.

Fetal development.–From eight weeks after

conception to birth, the fetus, generally considered less vulnerable than the embryo, is

subject to adverse influences likely to lead to

physical growth retardation and postnatal functional abnormalities. In experimental rodent

species, transplacental carcinogens are most

active during the latter half of gestation.

Infant development.–The infant may be

unusually susceptible to chemicals in a variety of

ways; for example, its immature metabolic

system may be unable to cope with foreign

substances or even with an excess of endogenous

substances.

Lactation. –Certain substances can decrease

the quantity of milk and alter its quality; others

may be excreted in the milk, rendering it

unpalatable to the infant; and still others may be

excreted in the milk that can have direct toxic

effects on the infant.

Postnatal function of the child.—Since

certain developmental processes are not complete until after birth–e.g., physical growth, and

structural and physiologic maturation of the

centraI nervous system and some endocrine

glands-it is to be expected that environmental

contaminants may detrimentally influence these

postnatal developments. Aside from observations on postnatal survival and growth rates,

little has been done in the way of experimental

studies on postnatal functional alterations induced by environmental chemicals. An exception is the increasing concern about behavioral changes that may be induced either by

prenatal exposure to substances for which the

pregnant mother is the intermediary or by direct

exposure of the immature child.

The latter aspects of the reproductive process have received more attention than the earlier

ones, for which there are no human data.

14
Teratogens

The cause of deviations occurring during

prenatal development that are not “normal

variants’’-i.e., not compatible with “normaI”

function in the offspring, and in which genetic

control is diverted from its normzd course by

additional factors—is a field of study that

requires urgent attention. Postconception events

connected with environmental factors, particularly chemical exposures, need emphasis. Diversion from normal embryonic and fetal development may take several forms. At the extreme,

development may cease altogether and the conceptus dies. In Iess extreme form there may be

retardation of intrauterine growth and development for some stage in gestation. Gross

structural or functional anomalies may accompany this phenomenon.

Over 80 percent of known clinical congenital

malformations and spontaneous abortions are

estimated to be of unknown etiology. Roughly

12 percent can be traced to genetic factors, with

a few percent more to known “environmental

insuhs.”s 5 By contrast, it can be shown in the

laboratory that a very broad range of chemical

agents can produce, under the proper conditions, some type of serious developmental

deviation. Thus, substances already found to be

embryopathic in animals range from highly toxic

substances such as anti-tumor drugs to commonplace consumer items such as aspirin.

Despite laboratory data indicating teratogenic potential for a wide variety of environmental factors in animals, only a few have been

proved or are strongly suspected to be embryopathic in man. The requisite epidemiologic

studies are lacking.

Those chemical factors known to be embryopathic in man include:

Methylmercury

Aminopterin

Thalidomide

Iodine deficiency (cretinism)

Steroid hormones with androgenic activity

Carbon monoxide (hypoxia)

Those factors strongly suspected of affecting

human prenatal development include: .

Cortisone

Vitamin A deficiency

Diethylstilbestrol

It has been difficult to obtain valid heahh

statistics reflecting prenataI health impacts. Data

on spontaneous abortion and the abnormalities

associated with abortion or other abnormal

pregnancy outcomes in selected groups will be

of great help. Among groups of special interest

would be those in which either parent had a

well-characterized occupational exposure.

Somatic Effects

Alterations in the reproductive processes by

exposure to certain environmental chemicals and

the unique effects of mutagens and especially

teratogens on the maternal-fetal biological unit

describe only the earliest aspect of developmental abnormalities. Data relevant to toxic effects

during reproduction are limited, compared with

the potential for data on impairment due to

somatic effects in the postnatal years. These

effects can be observed either relatively soon

after individual exposure or after periods ranging

from a few months to several years.,

Improper and insufficient nutrition still contributes to disease, disability, and death in a

great proportion of the world’s population. The

high frequency of malnutrition as soon asbreast

milk no longer serves as the sole source of food

combined synergistically with infections to

which this vulnerable age group is heavily exposed makes infant mortality and developmental abnormalities an important field for study.

In connection with dietary intake and environmental factors, the special vulnerability of

infants to methemoglobinemia should be

studied. Ingestion of nitrates or nitrites with

drinking water has been shown in infants 30-60

days old to be related to elevated methemoglobin levels.s G

Technological and social developments have

multiplied the hazards to which populations,

especially in urban areas, are exposed.37 Of

15
particular significance are the harmful effects of

chemicals on the central nervous system, whose

developmental process is not completed untiI

after birth. There is thus a critical period of

vulnerability during postnatal Iife and infancy.

In these stages of cerebral maturation, many

chemical compounds in common industrial use

can produce serious and irreversible damage. For

example, lead poisoning in children can produce

irreparable brain damage with permanent mental

retardation. A high degree of environmental

exposure often occurs in children in industrialized areas, and direct ingestion of Iead pigment

paints is also a major source of exposure.a 8

Peroneal nerve conduction velocity has been

shown to diminish with increasing blood lead

levels in children living in the vicinity of a

smelters 9

Studies of the effects on mortality and

morbidity of chronic exposures to air pollutants

strongly suggest that long-term exposure of

infants and children to air pollution can impair

respiratory health. Aggravation of chronic bronchitis, asthma, and pulmonary emphysema have

all been considered in association with community air pollution. There is evidence that

bronchitis can be caused by air pollution exposures over many years.40-42

To minimize the obvious importance of

smoking, occupation, and previous medical history on studies of respiratory mortality and

morbidity, a number of epidemiologic studies on

school children have been carried out. The

results of such studies indicate an increase in

respiratory illness in children who reside in areas

of high pollution, as compared with areas of low

pollution.4 3-45 It has been suggested that such

increased rates of iIlness cause higher rates of

chronic pulmonary disease in this population in

later life.

DISEASE RELATED TO iNGESTED WATER

POLLUTANTS OR CONSTITUENTS

Waterborne Diseases

During the period 1961-70, 130 waterborne

disease outbreaks occurred in the United

States.4G Waterborne disease outbreaks are no

longer on the decline in the United States as

indicated in table C.46947

per outbreak is indicated

The number of cases

in table D46’47 and

~he types of illnesses observed are Iisted in table

E. Two agents never before associated with

documented waterborne outbreaks in the United

States appeared during the 1961-70 period:

enteropathogenic Escherichirz coli (EEC), associated with adult disease, and Giardia lam blia.

The deaths reported over a 25-year period were

associated with chemical poisoning, typhoid

shigelIosis, amebiasis, enteropathogenic E. coli,

Table C. Average annual number of waterborne disease

outbreaks, by type of system: United, States, 1938-70

Years

All Public Private

systems systems systems

Number of outbreaks

1971-741 . . . . . . . . . . . . . . 25

1966-70 . . . . . . . . . . . . . . . 14

1961 -65 . . . . . . . . . . . . . . . 11

1956-60 . . . . . . . . . . . . . . . 12

1951 -55, . . . . . . . . . . . . . . 10

1946-50, . . . . . . . . . . . . . . 23

1938-45 . . . . . . . . . . . . . . . 38

221

4

3

5

3

6

12

4

10

8

7

7

17

26

lCraun, G. F., et al.: Review of the causes of waterborne

disease outbreaka in the U.S.–1971-1974. J. Am. Water Works

ASS C. 68(8): 420-424, Aug. 1976.

~Includes public and semipublic systems.

SOURCE: Craun, G. F., and McCabe, L. J.: Review of the

causes of waterborne disease outbreaks. Z Am. Water Works

Assoc. 65(1): 74-84, Jan. 1973.

Table D. Number of cases of waterborne disease per outbreak,

by type of system: United States, 1938-74

Ail Public Private

Years systems qmtems systems

Illness per outbreak

1971-741 . . . . . . . . . . . . . . 171 24,210 28

1866-70 . . . . . . . . . . . . . . . 114 166 93

1961 -65 . . . . . . . . . . . . . . . 680 2,603 39

1956-60 . . . . . . . . . . . . . . . 103 207 23

1951 -55 . . . . . . . . . . . . . . . 125 333 33

1946-50 . . . . . . . . . . . . . . . 114 292 43

1938-45 . . . . . . . . . . . . . . . 340 1,000 50

lCraun, G. F., et al.: Reviw of the causes of waterborne

disease outbreaks in the U.S.–1971-1 974. J. Am. Water Works

.’tSSOC.68(8): 420-424, Aug. 1976.

21ncludes ~“blic and semipublic sYstems.

SOURCE: Craun, G. F., and McCabe, L. J.: Review of the

causes of waterborne disease outbreaka. J. Am. Water Works

ASSOC. 65(l): 74-84, Jan. 1973.

16
Table E. Number of outbreaks and cases of waterborne disease, by type of system and illness: Unit

All systems Private

Illness out- Cases outbreaks breaks

Total . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130 46,374 95

Gastroenteritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 26,546 25

Infectious hepatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130 903 22

Shigellosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 1,666 16

Typhoid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 104

Salmonellosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

29 16,706 ;:

Chemical poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 46 7

EnteropathogenicE.co/i . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 188 4

Giardiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 176 1

Amebiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 39 2

Id States

ystems

Cases

6,564

4,498

664

939

104

96

42

188

19

14

1961-70

Public systems

outbreaks eese5

35 39,810

14 22,048

18 239

3 727

5 16,610

2 4

2 157

1 25

lone gastroenteritis outbreak also included 7 cases of infectious hepatitis.

20ne gastroenteritis outbreak was preceded by outbreak of 38 cases of Sahonelbsk.

SOURCE: Crasn. G. F.. and McCabe. L. J.: Review of thecauses ofwaterborne tisease outbreak. J. Am. Warer Works Assoc. 6S(l):

7484,Jan. 1973. -

salmonelIosis, and infectious hepatitis. Figure 2

shows the relationship between typhoid fever

and infectious hepatitis cases and shows that

while typhoid fever generally decreased infectious hepatitis increased.

One well-documented infectious hepatitis

outbreak involving 90 cases resulted from a

series of events including across-connection and

reduced pressure in the mains resulting from a

fire,48 Pkmtsproducingv eryclearw atert endto

show low bacterial counts accompanied by low

incidence of viral disease.lg Production of good

quality water should be measured by several

criteria, including filtered water turbidity, bacteria as indicated by plate counts and by

presumptive and confirmed coliform determinations, and use of chlorination. Plants treating

polluted water achieved low virus rates in cities

where’ qualified operators produced a superior

product. The investigation of the efficiency of

water treatment processes for the removal of

poliovirus Type 3 showed that with proper

conditioning of the water, removals of over 99

percent were attained.s 0

Clustering of multiple sclerosis patients in

Mansfield, Massachusetts, suggested that the

etioIogic agent was probably the water supply.51 It was hypothesized that exposure had

occurred when the patients were about 14 years

old, and the incubation period was estimated to

be about 23 years.

Fungi potentially pathogenic for man have

been isoIated from sewage and poIIuted water,s 2

and thus may affect the health of sewage

workers. Weil’s disease (leptospirosis) is held to

be a compensable disease as in infectious hepatitis. Occupational morbidity studies of sewage

i, Infectious hepatitis

!

----- Typhoid

i

~,

‘,, ./”--,

s#.-

\\,

‘.,

‘. —-.

I I I I 1 1

1946.50 1951.55 1956.60 1961.65 1966.70

YEARS

Figure 2. Average annual number of typhoid and hepatitis cases

occurring in waterborne outbreaks–1 946-70

17
workers can provide a guide for community

protection as welL

Water reuse. –Four factors relevant to the

utilization of recIaimed waters as a significant

portion of community water supply are microorganisms, toxic minerals, nontoxic minerals,

and stable organics. One articless focuses on the

stable organic fraction, and proposes that bioassay techniques may be the best available

means of assessing the toxicity of organics. In

areas with various types of water reuse, the

heahh statistics system should be systematically

monitored for comparison with control areas.

MUTATIONS

A disturbing type of laboratory data on

environmental heahh effects is the type dealing

with mutation, the persisting alteration of the

genetic materials in germ cells. Most of what is

known derives from pioneering studies of radiation effects on fruit flies.s 4 At present,

substantial advance has led to mutagenicity

testing by use of special bacterial strainss5 and

mammalian microsomes. A substantial number

of known environmentaI mutagens are also

carcinogens (135 out of 138 carcinogens tested

have been shown to be mutagens).

While concern about human mutation is real

and efforts to avoid it are biologically and

ethically justified, we have not actually demonstrated increased stable mutations in humans

due to environmental agents. What has been

shown is alteration in somatic mutational indexes such as increased chromosomal breaks in

lymphocytes as a result of exposure to ozone,

benzene, or radiation.

Nevertheless, there is reason to believe that a

proportion of birth defects is due to mutations,ss and that more vigorous applications of

epidemiological procedures may be able to

demonstrate gradients that may reflect environmental exposures.

The health statistics system may make a

useful contribution to the control and prevention of mutation by establishing improved procedures for detection and analysis of genetically

related birth defects in human populations.

EPIDEMIOLOGIC METHODS

APPLICABLE TO ENVIRONMENTAL HEALTH

A very brief overview is now offered of the

methods of epidemiology and their more useful

applications to national health data systems,

particularly for identifying and assessing environmental health hazards.s 6

DATA AVAI LABLEFOR ANALYSES

Epidemiolo@c analysis of health measurements by age, race, sex, place, and time is the

customary initial approach to describing any

problem within the context of this report. The

epidemiologic measures for any given disease

may be incidence, prevalence, case fatality, or

mortality. Temporal and spatial variation may

reflect exposure and response to environmental

pollutants. Epidemiologic analysis is also applicable to variations in states of health, as in

pulmonary function, cholinesterase levels, or

body burden estimates based on blood, lead,

carbon monoxide, or arsenic, lead, or mercury in

hair or nails.

Stratification of a population into broad age

groupings by life epochs (infancy, preschool,

school, adult, retirement) provides subsets that

obviously differ in many parameters–

physiological, psychological, and social; however, they also differ grossly in their usual range

of activity and potentials for exposure to different and unique Iocal environments. Demonstrations of excesses of diseases and/or rapid

changes within one but not others of these

groups provide biologic populations indicators

of responses to changing environments. The

coincident decreases in infant and childhood

death rates and increases in adult mortality from

coronary heart disease, cancer of the lung, and

18
chronic obstructive pulmonary disease, particularly in white males, are graphic illustrations of

this phenomenon occurring over a period of

decades. A similar, more rapid change in blackwhite ratios of the same diseases has occurred–

white excesses for some cancer sites, nationally

at the time of the 1950 census, were repIaced by

black excesses by 1967.s 7 Several competing

hypotheses are raised: black entry into the

urban-industrial environmental complex leading

to increased exposure to deleterious physiochemical agents; increased stress of the modern,

affluent society as one of the prices to be paid

for equal opportunity; and change in smoking

patterns of black males.

The collection and analysis of routine vital

statistics identifies some of these phenomena;

their explanation requires more detailed information, possibly coming from secondary analysis of morbidity data over time in relation to

person characteristics (such as that in Social

Security Administration files, described in appendix IV). Although definitive answers almost

invariably require ad hoc epidemiologic studies,

much in the way of identification of problems

and generation of hypotheses can be achieved by

the analysis of data collected primarily for other

purposes.

GROUP COMPARISONS

In general, epidemiological methods appropriate for use in examining environmental health

problems are of two types. The first type

involves comparisons between an exposed and a

control group, or among groups with gradients in

exposure. The second is concerned with comparisons within a group whose exposure varies

over time.

The between-group comparison may involve

groups which differ in exposure because of their

place of work, their occupation, or other circumstances related to their way of life, for

example, a particular hobby (as in exposure to

lead in making pottery), or a personal habit

(such as smoking, diet, consumption of drugs or

medication). Alternatively, however, differences

in exposure may be defined in terms of the

general community or geographic area, such as

exposure to community air pollution or community water supplies. The greatest problem in

doing a study comparing the health experience

of two or more groups is their comparability

with respect to other significant variables. This

can be approached by matching individuals on

some of the more important and easily ascertained characteristics, such as age, sex, economic

status, ethnic group, and smoking habits. Matching on relatively straightforward variables, however, involves a preliminary census to obtain the

information necessary for matching; and this

must then be followed by the actual matching

and sample selection and by whatever procedure

is suitable for obtaining data on the variables

involved in the hypothesis being tested. More

commonly, exposed and control populations are

selected which are believed on more general

evidence (for example, census data) to share

about the same demographic characteristics but

to differ with respect to the variables of primary

interest (e.g., exposure to air pollution).

Random sampling is then relied upon to prevent

significant bias with respect to other background

variables. Usually, information is also collected

on these variables, and, if the two groups differ

significantly, the variables are taken into account during analysis of the data, either by

making comparisons within subgroups of the

exposed and control groups (which requires

larger sarnpIe sizes than would ot$erwise be

needed) or by multivariate statistical analysis.

An alternative to defining the groups in

terms of exposure is to define them in terms of

effect, looking for differences in exposure which

may discriminate among the groups.

In contrast to between-group comparisons,

the study of an exposed group over time

involves using the group as its own control, thus

avoiding the problem of obtaining comparable

exposed and control population groups. However, characteristics of these groups can change

over time. The comparisons are made of variation of he’dth experience of the group with

variation in environmental exposure. This

method is applicable principally to acute effects

since it may involve rapidly fluctuating exposure, as in day-to-day variation in exposure to air

pollution. One of the analytical problems aMociated with this method is that of handling

temporal variation of both health effects and

environmental exposure. For example, seasonal

19
variation in morbidity or mortality occurring

coincidentally with seasonal variation in exposure may or may not indicate causation.

COMMUNITY EXPOSURE VERSUS

OCCUPATIONAL EXPOSURES

The first evidence that some aspect of the

environment is associated with a deleterious

effect on health often occurs in an occupationally defined group. Recognition of the association is a function of several factors characteristic of the occupational setting: (1) the group is

defined and accessible to followup; (2) the

exposure is uniform, or similar, for the defined

group; (3) the exposure may consist of substances different from those experienced by the

general population; and (4) the exposure may be

to a higher concentration than that experienced

by the general population, resulting in more

clearly definable health effects.

Community exposures, in contrast, tend to

be: (1) associated with groups that are poorly

defined and difficult to follow; (2) diffuse and

variable over a geographically defined group; (3)

related to substances at levels difficult to measure for general population exposure; and (4)

related to low levels of concentrations which

result in subtle or long term, if any, health

effects.

However, once a substance has been shown

to have health effects in an occupational or

other environmental setting, it is proper to be

concerned with the possible health effects of

community exposures to low concentrations

(for example, exposure to asbestos). In addition,

community exposures may occur which have no

analog in the workpIace (exposure to community air pollution, to nitrates in drinking water).

HEALTH EFFECTS AND

COMMUNITY EXPOSURES

The term “community exposure” is used in

this report to refer to individuals whose exposure is not limited to the workplace. It includes

subgroups of the population which might be at

special risk because of other exposures or

unusual susceptibility. These groups might include, for example, those with proximity to a

point source, and individuals of specific sex, age,

ethnic backgrounds, or economic status, which

could result in more than usual exposure to

certain foods, types of housing, or greater

susceptibility to the effects of nitrates in drinking water or to chronic respiratory disease.

Approaches to studying the relationship

between health and environmental exposures in

the community may be classified in several

ways, for example, according to the method of

selecting the population at risk, according to the

analytic method to be employed, or according

to the kinds of contrast to be made. For

convenience, these will be discussed here under

the following headings: geographic comparisons,

comparisons over time, and dose-response relationships. A study may, of course, employ a

combination of these.

Geographic Comparisons

Geographic comparisons are those in which

the exposure is defined by geographic area.

Thus, for example, the health experience of

individuals living in areas with heavy air pollution may be compared with the health experience of individuals living in lightly polluted

areas. One shortcoming of this kind of study is

that a single measure or combination of measures of exposure is used to represent exposure of

the entire group within each area. The contrasts

studied may consist of high-low comparisons

between two areas, or of a gradation of exposures using several areas.

If a measurement is available of the effect of

a pollutant on each individual, the analysis may

consist of testing for the differences in mean

values between areas. The possibility also exists

of using geographic comparisons to estimate a

dose-response relationship by quantifying the

exposure for several areas and testing for a

significant gradient. In interpreting apparent

geographic differences in health, it is important

to take into account the possible differences in

factors other than the one of primary interest.

Migration and retirement rates in particular need

to be considered when possible.

Comparisons Over Time

Comparisons over time are those in which

the exposure is described primarily in terms of a

I

20
time interval. In air pollution studies, for example, one may relate health effects to pollution

measurements representing a day (or less), a

week, a month, a year, or longer. For intervals

of less than a year, seasonal variation in both

‘ exposure and effect must be taken into account

since coincidental seasonal variation could imply

a relationship which may or may not represent a

causative effect. Usually a relatively short time

interval is used since pollution may vary greatly

over time. The week seems to be a reasonable

compromise since the day-of-the-week effect in

morbidity and mortality can then be discounted.

Usually correlation and regression analysis are

used since the number of exposure-effect pairs

tends to be large and represents many gradations

of exposure. However , some kind of seasonal

adjustment is usually necessary. As with geographic comparisons, it may be possible to

estimate dose-response relationships provided

enough levels of exposure are measured.

Temporo-Spatial Comparison

The combination of geographic comparisons

with comparisons over time offers several advantages. First, if the same variation over time in

relation to pollution is found in several areas, it

suggests that the phenomenon does not result

from variation with a third concomitant variable

peculiar to a single situation. Similarly, geographic differences may be found to exist

regardless of relatively small time variations in

exposure. And finally, it may be found that a

stronger effect of temporal variations may occur

in more heavily polluted areas. Thus temporospatial analysis tends to yield more specific

indexes of environmental effect than do either

geographic (spatiaI) or comparisons over time

(temporal).

Dose-Response Relationships

The study of dose-response relationships

usually involves estimating exposure for individuals, rather than for groups,. and relating this

exposure to indices of health, both exposure and

effects being measured on a continuous scale or

at least one with many possible values. Estimation of the relationship itself then consists of

fitting a curve to the data points. This could also

be done with grouped data. In both these

methods, observations are usually taken directly

on individuals rather than by assuming a uniform exposure on the basis of geographic location or exposure during a given period of time.

For example, one might start by measuring the

exposure of each individual to carbon monoxide

by use of some sort of personal monitoring

method; and measuring such effects as change in

carboxyhemoglobin or expired air carbon monoxide concentration or visual acuity. Thus, a set

of two individual measurements is obtained for

each person. As described previously, doseresponse analysis can also be carried out on data

geographically defined or using a temporal sequence, but exposure data then become less

precise.

EPIDEMIOLOGIC MONITORING

AND SURVEILLANCE

Surveillance is defined here as collecting and

arudyzing data as it becomes available in a time

sequ-enc; in order to detect departures from

some established or expected value or norm. In

the context of environmental health, departures

from normality in either exposure (as in air

pollution) or health effects are of interest. The

goal is to be able to take useful and timely

corrective action. In order to determine when

departures from normality occur, expected

values must be calculated along with an estimate

of variance to provide confidence limits. One

could then determine whether deviations of

environmental variables are associated with morbidity or mortality. Conversely, departures from

expected vzdues of morbidity or mortality might

indicate the need to look for variations in

environmental exposure variables.

EFFECT OF INTERACTIVE AND

CONTRIBUTORY VARIABLES

The importance of taking into account

variables other than those of primary interest

was mentioned earlier in the discussion of

geographic variation. These variables may themselves be environmental, or may be other characteristics of the individuals being studied. One

may wish merely to “control for” or eliminate

the effect of other factors known or suspected

to have an effect, or alternatively, these factors

may be of interest in themselves, either in terms

21
of their own effect, or to detect interactions

between them and the primary variable. The

method of analysis depends upon the choice

among these alternatives. If control of the other

variables is the main objective, then a standardization procedure may be used, the analysis may

proceed within several categories of the variables, or multivariate analysis may be used. If

the effect of these variables themselves is an

objective, then multivariate analysis may be

preferred.

RARE EVENTS

In looking for environmental influences on

health, one also needs to consider the rare health

event. Rare events may result from environmental exposures, but because data need to be

accumulated over long time periods or in large

populations to detect an increase, associations

may be particulady difficult to establish. What

appear to be rare events, however, may not

actually be rare; they may result from errors in

coding or diagnosis of a common event. Furthermore, they may be overlooked because of

lack of specificity of coding, either because they

tend to be grouped with more common conditions for coding purposes or because they

cannot be distinguished from them because of

lack of information. For example, the information recorded on the death certificates may not

be adequate for coding, as in the case of

mesothelioma of pleura or peritoneum and

angiosarcoma of the liver, both of which require

specification of cell type. In other cases the

mechanism by which a condition develops needs

to be described in addition to a physical

description of the result.

HEALTH EFFECTS AND

OCCUPATiONAL EXPOSURES

Existing Records

Death certificates, in spite of their shortcomings, are a useful source of information on

occupational mortality. However, they currently

show “last” occupation rather than “usual”

occupation. Studies are needed to determine the

extent this reflects the major, or at least a

significant, occupational exposure. This can be

deduced to some extent by comparing length in

last occupation, also available on the death

certificate, with age. Other alternatives are to

compare data from death certificates with information from next of kin, social security

information, or union records. Given that the

occupation as shown on the death certificate has

some validity, the next problem is to code and

tabulate the information in such a way that

occupational risks are adequately reflected.

Several codes are now in use, and comparative

work is being carried out to evaluate their

usefulness. It is equally important to obtain and

code information on industry worked in, since

this may reflect occupational risks, in a more

valid way, than occupation per se. One further

step would be to code hazardous substances to

which a worker has been exposed.

Special Ascertainment of Exposure

Detailed occupational histories should be

obtained from cancer registries, union records,

or social security records. An example of the

latter can be found in statistical reports of

occupation of disabled workers by cause of

disability.s 8 Interviews of surviving employees

or of next of kin can be used to obtain fairly

detailed histories, but these are time consuming

and depend to a large degree on memory.

Furthermore, interviews must be carefully

structured so that information of the desired

specificity is obtained. One approach is to first

obtain a detailed chronological history; follow

this with a check list of occupations and

industries of special interest; and finally to

inquire about exposures to known or suspected

toxic substances. Standardized procedures for

such work have been developed in a few centers,

and need to be more generally utilized.

o

22

00
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9Baginsky, E.: Occupational illness and accidents

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] ‘U.S. Department of Health, Education, and Welfare:

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13 U.S. Department of Health, Education, and Welfare:

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14U.S. Department of HeaIth, Education, and Wel&re:

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3oCenter for Disease Control: Adult Use of Tobacco–

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31 Kuller, L. H.: Epidemiology of cardiovascular diseases: Current perspectives. Am. J. Epidemiol. 104:

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34 Heyden, S.: The hard facts behind the hard-water

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damage and risk assessment, in Evaluation of Chemical

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36Shearer, L. A., et al.: Methemoglobin levels in

infants in an area with high nitrate water supply. Am. ./.

Public Health 62:1174-1180, Sept. 1972.

37 Panel on Chemicals and Health Report of the

President’s Science Advisory Committee: Chemicals and

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1973.

38National Academy of Sciences, National Research

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39 Landrigan P.: Increased lead absorption with anemia

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1975.

40 Douglas, J. W. B., and Wailer, R. E.: Air pollution

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41 Lunn, J. E., Knowelden, J., and Handyside, A. J,:

Patterns of respiratory illness in Sheffield infant school

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A follow-up study. Br. J. Rev. Sot, Med. 24:223-228,

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44 C011ey, J. R, T., and Reid, D. D.: Urban and social

origins of childhood bronchitis in England and Wales. Br.

Med. J. 2:213-217, Apr. 1970.

45 Zap]etd, A., Jech, J., Paul, T., and sam~ek~ M,:

Pulmonary function studies in children living in an

air-polluted area. Am. Rev. Respir. Dis. 107: 400-409,

Mar. 1973.

46 Craun, G. F., and McCabe, L. J.: Review of the

causes of waterborne disease outbreaks. J. Am. Water

Works Assoc. 65(l): 74-84, Jan. 1973.

47 Craun, G. F., et al.: Review of the causes of

waterborne disease outbreaks in the U.S.–1971-1 974. J.

Am. Water Works Assoc. 68(8): 420-424, 1976.

48 Taylor, F. B.: The Holy Cross episode. J, Am. Water

Works Assoc. 64(4): 230-232, Apr. 1972.

4gHudson, H. E., Jr.: High quality water production

and viral disease. J. Am. Water Works Assoc. 54(1 O):

1265-1272, 1962 and Woodward, R. L.: Discussion. J.

Am. Water Works Assoc. 54(10): 1271-1274, Oct. 1962.

5oRobeck, G. G., Clarke, N. A., and Dostal, K. A.:

Effectiveness of water treatment processes in virus

removal. J. Am. Water Works Assoc. 54(1 O): 1275-1290,

Oct. 1962 and Hartung, H. O.: Discussion. J. Am. Water

Works Assoc. 54(10): 1290-1292, Oct. 1962.

51 Eastman, R., Sheridan, J., and Poskanzer, D. C,:

Multiple sclerosis clustering in a small Massachusetts

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before onset. N. Engl. J. Med. 209 (15): 793-794, Oct.

11, 1973.

52 Dixon, F. R., and McCabe, L. J.: Health aspects of

wastewater treatment. J. Water PoUut. Control Fed.

36(8): 984-989, Aug. 1964.

5SOngerth, H. J., Spath, D. P., Crook, J., and

Greenberg, A. E.: Public health aspects of organics in

water. ]. Am. Water Works Assoc. 65(7): 495-498, July

1973.

54 MuIler, H. J.: Artificial Transmutation of the Gene.

Science 66:84, 1972. pp. 84-87.

55~eq B. N<,McC_, J.,ad yama&i, )7.:Methods

for detecting carcinogens and mutagens with the salmonella/mammrdian-microsome mutagenicity test. Mutagen

Res. 31:347-364,

56 GoMsmith, J.

in environmental

1975.

R.: Statistical problems and strategies

epidemiology, in L. M. LeCam, J.

24
Ncyman, and E. L. Scott, eds., Proceedings of the Sixth

Berkeley Symposium on Mathematical Statistics and

?+obability, Vol. VL Berkeley, University of California,

1972. ch. 1.

57 Burbank, F., and Fraumeni, J. F., Jr.: U.S. cancer

mortality: Nonwhite predominance. j. NatL Cancer Inst.

49:649-659, Sept. 1972.

580ccupational Health Program and Social Security

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Earnings. Ann Arbor, Mich., May 1974. Unpublished.

25
I

1.

2.

3.

4.

5.

6.

7.

8.

LIST OF DETAILED TABLES

Definite and possible health effects of environmental pollutants and exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27

National primary ambiant airquality standards . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28

Exposure estimates, selmted harmfil effects, anddate ofcriteria document forsetected occupational a~nts . . . . . . . . . . . 30

Percent distribution of cancers at selactad sites for which thare ara sound atiologic hypotheses . . . . . . . . . . ., . . . . . . . . 31

Carcinogenic agents that may be associated with various occupations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

Standardized mortality ratios for all sites of cancer combined, and for cancer of selected sites for white males aged 20-64

years, by broad occupational group: United States, 1950 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33

Prevalence of chronic bronchitis reported in health interviews, by age, family income, and place of

residence: United States, 1970 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33

Prevalence of emphysema reported on the basis of physicians’ diagnosis in haalth interviews, by age, family income, and

place ofresidence: United States, 1970. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34

26
Table 1. Definite and possible health effecte of environmental pollutants and exposures

[Items in parentheses refer to effects other than those directly affecting human health status]

Agent, pollutant, or source I

Definite effect Possible effect

COMMUNITY AIR POLLUTION-A

Sulfur dioxide (effects of sulfur oxides maybe due to

sulfur, sulfur tdoxlde, sulfuric acid, or sulfate salta)

Sulfur oxides and particulate matter from combustion

sources

Particulate matter [not otherwise specified)

Oxidants

Ozone

Carbon monoxide

Nitrogen dioxide

Lead

Hydrogen sulfide

Mercaptans

Asbestos

Organophosphorus pesticides

Other odorus C0mDo0nd9

Beryllium

Airborne microorganisms

Bacteria

Vmmas

Protozoa and metazoa

Metals

Nitrates

“Softness” factor

Sulfates andlor phosphates

Fluorides

1,

2.

3.

4.

5.

6.

7.

8.

11.

12.

13.

15.

17.

23.

25.

26.

Aggravation of asthma and chronic bronchitis

Impairment of pulmonary function

Sensory irritation

Short-term increase in mortality

Short-term increase in morbidity

Aggravation of bronchitis and cardiovascular

disease

Contributory role in etiology of chronic bron.

chitis and emphysema

Contributory role to respiratory disease in

children

Aggravates emphysema, asthma, and bronchitis

Impairs lung function in patients with bronchitisemphysema

Eye and respiratory irritation and impairment in

Derform ante of student athletes

Impairs lung function

Impairs exercise tolerance in patients with cardio

vascular disease

Increased storage in body

fncreased mortality from acute exposures

Causes sensorv irritation

26. Produces pleural calcification

29. Malignant mesothelioma, asbestosis

31. Acute fatal poisoning

32. Acute illness

33. Impaired cholinesterase activity

35. Besylliosis with pulmonary impairment

36. Airborne infections

FOOD AND WATER CONTAMfNANTS-B

1. Epidemic andendemic gastrointestiw4 in feotimo

(typhoid, cholera, shigallosis, salmonellosis,

Ieptospirosis, etc.)

3. Epidemic hepatitis andothervird infections

5. Amoebiasis, achistosomiasis, hydatidosis a”dothel

parasitic inactions

6. Lead poisoning

7. Mercury poisoning (through foodchains)

6. Cadmium poisoning (through food chains)

9. Arsenic poisoning

10. Chromium poisoning

13. Methemogloblnemia (with bacterial interactions)

16. Gastrointestinal hypermotility

16. Fluoro.?is ofteeth wften in excess

9. Contributorv role inetiologv oflungcencer

10. “’lncraase in chronic respiratory disease

14.

16.

16.

19.

20.

21.

22.

24.

27.

30.

Increased probability of motor-vehicle accidents

Acceleration of aging, possibly due to lipid peroxidation and related processes

Increased general mortality and coronaw mortality rates

Impairment of central nemom systcm function

Causal factor in atherosclerosis

Fcctor in pulmonary emphyasma

fmpaimsent of lung defenses such as meat cells

and mccrophages or altered lung function

Impairment of hemoglobin and porphyrin syn.

thesis

Headache, nausea, and sinus affac$ions

Ca_,.;S.II,?~ to chro”i~ ~“lmo”a~ di$e~e (~&stos and lung cancer]

34. Headache and sinus affections

2. SccondaW interaction with malnutriti$m and with

nitrates in water (cf., no. 15)

4. EVe and skin inflammation from swimming

11. Epidainic nephropathy

12. “Blcckfoot” disease

14. Increase in cardiovascular disaase

27
Table 1. Definite and possible health effects of environmental pollutants and exposures-Con.

[Items in parentheses refer to effects other than those directly affecting human health status]

Agent, pollutant, or source I

Definite effect

I

Possible effect

LAND POLLUTION–C

Human excreta

.

Sewage

Industrial and radioactive waste

Pesticides-lead arsenate

Cold damp

Cold dry

Hot dry

Hot damo

Natural sunlight

Diagnostic X.ray

Therapeutic radiation

Industrial uses ofradiation andmining of radio.

act ive ores

Nuclear power and reprocessing plants

Microwaves

Traffic

Aircraft (including sonic boom)

1.

3.

4.

1.

3.

5.

7.

8.

9.

10.

11.

12.

14.

15.

16.

17.

18.

1.

2.

3.

4.

6.

9.

10.

14.

15.

16.

17.

2.

Schistosomiasis, taeniasis hookworm, a“d other

infections

Storage and effects from toxic metals and other

substances through food chains

Increased storage of heavy metals in smokers of

tobacco grown on treated areas

THERMAL EXPOSURES–D

Excess mortality from respiratory disease and

fatal exposure

Excess morbidity from respiratory and related

diseases and morbidity from exposure

Mortality from frostbite and exposure

Morbidity from frostbite and respiratory disease

Heatstroke mortality

Excess mortality attributed to othar causes

Morbidity from heatstroke and from other causes

Impaired function; aggravation of renal and circulatory diseases

Increase in skin affections

Heat-exhaustion mortality

Excess mortality from other causes

Heat-related morbidity

Impaired vigor and circulatory fu”ctio”

Aggravation of renal and circulatory disease

RADIATION AND MICROWAVES-E

Fatalities from acute expmmre

Morbidity due to “burn”

Skin cancer

Interaction with drugs in susceptible individuals

Skin cancer and other skin changes

Skin cancer

Increase in leukemia

Acute accidental deatha

Radiation morbidity

Uranium nephritis

Lung cancer in cigarette-smoking miners

NOISEANDV18RATIONS-F

Permanent hearing loss

2.

2.

4.

6.

13.

5.

7.

Typhus, plague, Ieptospirosis, and other infec.

tious diseases

Contributes to excess mortality and morbidity

from othar causes

Rheumatism

Impaired lung function

Increase in prevalence of infectious agents and

vectors

Increase in malignant melanoma

Contributing factors to leukemia

8. Alteration i~fecundity

11. Increase in other cancers

12. Acceleration ofsging

13. Mutagenesis

18. lncre&se in8djacent cc+nmunity morbidity or

mortality

19. Increese in cancer incidence

20. Community disaster

21. Alteration inhuman gmmticmateria[

22. Tissue damage

1. Progressive hearing leas

3. Aggravation orcause ofmentilii!ness

4. Atiicular andm”S”lardiseSe

5. Adverse effects onnewoussystem

28
Tablel. Definite andpossible health effects ofenvironmental pollutan~and exposures-Con.

[Items in parentheses refer to effects other than those directly affecting human health status]

Agent, pollutant, or source Definite effect Possible effect

HOUSING AND HOUSEHOLD AGENTS–G

Heating, cooking, and refrigeration

Fumes and dust

Crowding

Structural factors (including electrical wiring, stoves,

and thin walls)

Paints and solvents

H:i~:~:old equipment and supplies (including pestiToys, beads, and painted objects

Urban design

1. Acute fatalities from carbon monoxide. fires and

explosions, and discarded refrigerators

3. Acute illness from fumes

4. Aggravation of asthma

6. Spread ofacute andcontribution to chronic

disease morbidity and mortality

7. Accidental fatality

8. Accidental injury

9. Morbidity andmortality from lack of protection

from heat or cold

10. Morbidity andmortality duetofire or explosion

11. Childhood lead.poisoning fatalities, associated

mental impairment, and anemia

12. Renal andhepatic toxicity

13. Fatalities

14. Fatalities from fire and injury

15. Morbidity from fire and injury

16. Fatalities from poisoning

17. Morbidity from poisoning

18. Mortality andmorlridity

19. Increased accident risks

2. Increase indiseases of therespiratory tract in

infants

5. Increase inchronic respiratory disease

20. Contribution to mental illness

Table2. National Drimarv ambient airauality standards

Pollutant

Carbon monoxide, . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Hydrocarbons (nonmethane). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Nitrogan dioxide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Photoch6mical oxicfents, . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Particulate matter .,,...,. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Sulfurdioxide .,.....,. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

lNot to be exceeded more than once Per Year.

2As ~ guide in de~sing implementation plans for achieving oxidant standards.

Averaging

time

1 hour

8 hours

3 hours

(6 to 9 a.m.)

1 year

1 hour

24 hours

24 hours

24 hours

1 year

Frequency

parameter

Annual maximum’

Annual maximum

Annual maximum

Arithmetic mean

Annual maximum

Annual maximum

Annual geometric

mean

Annual maximum

Arithmetic mean

Concentration

pg/m3

40,000

10,000

2160

100

160

260

75

365

80

ppm

35

9

20.24

0.05

0.08

,..

. . .

0.14

0.03

SOURCE: EPA Regulations 40CFR50; and Commerce Chewing House, Inc.: PolzutionC~nfy~/Guide, 1974.

29
Table3. Exposure estimates, selwted harmful effects, andtite ofcriteria document forsalwted occupationaIa@nts

Substance or agent

Noise . . . . . . . . . . . . . . . .

Lasers . . . . . . . . . . . . . . . .

Hot environments . . . . . . . .

Ultraviolet radiation . . . . . .

Inorganic lead . . . . . . . . . .

Carbon monoxide . . . . . . . .

Inorganic mercury . . . . . . .

Beryllium and its compounds

(Ethyl) parathion

Methyl parathion

Coal tar, pitch . .

Benzene . . . . . .

Fluorides . . . . .

Chromium . . . .

. . . . . . . .

. . . . . . . .

. . . . . . . .

. . . . . . . .

. . . . . . . .

. . . . . . . .

Boron trifluoride and

other compounds, boron . .

Arsenic . . . . . . . . . . . . . . .

Carbon tetrachloride ., . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . .

Cadmium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Exposure

estimate

7,500,000

120,000

1,300,000

320,000

83,000

2,000,000

150,000

30,000

250,000

150,000

50,000

2,rXJo,ooo

350,000

160,000

50,000

1,500,000

160,000

100,000

Selected harmful effects

Hearing andcommunications

impairment

Cataract

Heat stroke, heat exhaustion

Sunburn, eye irritation,

skin cancer

Colic, neurological impairment,

anemia

Impairment of oxygen transport

by blood

Stomatitis, tremor, psychic

disturbance

Respiratory irritation and

granuloma, chronic changes in

other organs, possibly cancer

Headache, sweating, coma

Skin irritation and sensitization,

possibly cancer

Bone marrow depression, leukemia

Respiratory, eye and skin irritation

Skin irritation, sensitization,

ulcer, possibly cancer

Chest symptoms, central narvous

symptom reactions

Skin reactions, sensitization,

possibly cancer

Liver and kidney failure

Gastrointestinal irritation,

kidney disease, possible

emphysema from inhalation

Date of criteria

Iocument if available

1972

. . .

1972

1972

1973

1972

1973

1972

. . .

. . .

1974

1975

1975

. . .

1975

. . .

. . .

30
Table4. Percent distribution ofcancem atsel=ted sites forwhich there aresound etiologic hypotheses

Site

Mouth (140,141,143,144) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Salivary gland (142) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Esophagus (150) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Stomach (151), . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Colon and rectum (153,154) . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Liver (155.0) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Liver (155.0) Africa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Lung(162) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Breast (170) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Cervix uteri (171) . . .. m...... . . . . . . . . . . . . . . . . . . . . . . . . .

Corpusuteri (172) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Ovary (175) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Otherfemalegenitals (176)..,,.. . . . . . . . . . . . . . . . . . . . . . . . .

Prostateandtestis (177,178)..,.. . . . . . . . . . . . . . . . . . . . . . . . .

Penis (179.0) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Bladder (181.0) Western industrial . . . . . . . . . . . . . . . . . . . . . . . . .

Bladder (lB1.O) Africa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Skin (190,191) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Braintumors (193) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Leukemia and Iymphoma (200-205)

Children . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Adults, . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Percent distribution

90

80

4

70

80

50

1

1-2

<1

10-20

2

<1

<1

2

<7

<1

5

4

1

1

1

*8

95

50

80

<1

<1

10

<1

1

<6

100

*I5

95

98

30

100

<lo

100

100

100

100

99

100

<5

30-40

50

<8

98

92

99

SOURCE: HigQnson, J., and Muk, C.: Epidemiology, in J. Higghson, ed., Cancer Ilfedichre, New York. Lea& Febiger, 1974.

31
Table5. Carcinogenic agents thatmaybe

Agent

Specific agents:

Arsenic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Coal tar,pitch . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Petroleum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Shaleoils . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Lignitetar,paraffin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Creosoteoils . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Anthraceneoils . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Sootcarbonblack . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Mustardgas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Cutting (mineral) oils . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Productsofcoal carbonization . . . . . . . . . . . . . . . . . . . . . . . .

Sunlight . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Chromates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Asbestos . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Aromatic amines, dyes,chemicals used in rubber industry . . . . . .

X-rays, radium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Nickel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Benzol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Isopropyl oil . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Radioactivechemicals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Chemicals (various) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Vinyl chloride . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Nonspecific (occupations):

Wood furnitureworkem . . . . . . . . . . . . . . . . . . . . . . . . .. . . . .

Leatherworkers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . .

Softcoal workers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Machinists, sheet metal workers,

carpenters, construction painters . . . . . . . . . . . . . . . . . . . . . .

mciated with various occupations

Sites of cancer

Skin, lung

Skin, lung

Skin, lung

Skin

Skin

Skin

Skin

Skin

Lung

Skin, possibly respiratory and

upper alimentary tract

Lung, bladder

Skin

Lung

Lung, pleura, peritoneum,

gastrointestinal tract

Bladder, possibly biliary

tract, salivary glands

Skin, lung, leukemia

Lung, nasal cavity and sinus

Leukemia

Lung,laWnx, nasal sinus

Bones, nasal sinus

Lymphoma, pancreas

Liver

Nasal cavity, sinuses

Nasal cavity, sinuses, bladder

Stomach

Lung

Areas where noted

United States, Great Britain,

Germany, France,

Argentina, Taiwan,

African countries

United States, Great Britain

United States, France, Great

Britain, Austria

United States, Great Britain

Great Britain, France

United States, Great Britain

Great Britain

United States, Great Britain

Japan

Great Britain, Australia

Great Britain, United States,

Japan

United States,Argentina,

Australia, France, et al.

United States, Great Britain,

Germany, Canada

United States, Great Britain,

Germany, Canada, S. Africa,

Holland, Australia, USSR,

Italy, et al.

United States, Germany, Great

Britain, Switzerland, et al.

United States and many

other areas

Great Britain, Norway,

Canada

United States, et al.

Unitad States

United States

United States

United States, Germany,

Sweden, et al.

Great Britain, United States

Great Britain, United States

United States(l report)

United States, G rest Britain

SOURCE: Modified from Levin, D. L., Devesa, S. S., Godwin, J.D., andSilverrnan,D. T.: CancerRatesand Risks. DHEWPub. No.

(NIH) 75-691. Washington. U.S. Government Printing Office, 1974.

32
Tabl@6. Standardized mortality ratio$for all sites of cancarcombined, and for cancer of selected sites for white males aged 20-S4vears. bvbroad occuDationalwouD:

United States, 1950

r

Buccal

All cavity Esopha. Larg+ Lung Leukemia

sites and gus

Stomach Rectum and intestine Bladder Ski n and aleupharynx bronchus kemia

Broad occupational group

Standardized mortality ratios

All persons, aged 20-64 . . . . . . . . . . . . . . . . . 100 100 100 100 100 100 100 100 100 100

Professional, technical, and kindred vmrkers . . . . . . . . . .

Farmers and farm managers . . . . . . . . . . . . . . . . . . . . .

Managers, officials, and proprietors, except farm . . . . . . .

Clerical andkindred workera . . . . . . . . . . . . . . . . . . . .

Salmworkera. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Craftsmen, foreman, and kindred workers . . . . . . . . . . . .

Oparatlve and kindred workers . . . . . . . . . . . . . . . . . . .

Service workers, except private household ., ., ., . . . . . .

Laborers, including farm laborers rmd foremen . . . . . . . .

Farm laborers and foremen . . . . . . . . . . . . . . . . . . .

Laborers, except farm and mine . . . . . . . . . . . . . . . .

91

81

%

102

111

101

109

105

59

123

83

62

S3

100

93

107

105

141

133

84

161

6S

35

64

77

70

117

1z

149

166

S5

182

64

91

:

75

108

102

102

116

79

130

124

81

110

11s

114

104

105

106

95

53

108

111

64

94

103

113

11s

111

119

94

32

113

62

55

95

94

103

132

110

125

103

53

123

97

73

B5

115

111

125

99

123

96

76

104

93

133

105

93

137

132

12s

.-

213

.-

172

114

127

111

93

106

105

92

&

72

106

SOURCE: Levin, D. L., Devesa, S; S., Godwin, J. D., and Silverman, D. T.: Cancer’Rates and Risks. DHEW Pub. No. (NIH) 75.691. Washington. U.S. Government

Printing Office, 1974,

Table7, Prevalence of chronic bronchitis reported in health interviews, by ege, family income, and place of residence: United States,

1970

Family income and place of residence

Rate per 1,000 persons

Total . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32.7 38.9 23.2 35.4 41.2

_

Family income

Leaathan $3,000 . . . . . . . . . . . .

$3,000%$4,999 . . . . . . . . . . . . .

$5,000-$6,999 . . . . . . . . . . . . .

$7,000-$9,999 . . . . . . . . . . . . .

$10,000-$14,999 . . . . . . . . . . . .

$15,0000 rmore . . . . . . . . . . . .

39.5

35.0

31.0

32.3

32.6

30.8

33.0

31.9

33.8

33.0

24.9

30.0

36.2

36.4

37.9

46.9

38.8

39.8

35.4

43.1

38.5

26.0

28.3

26.4

17.6

25.3

21.8

23.7

24.0

24.0

24.0

22.2

●

54.6

34.3

43.4

35.3

28.0

30.3

34.3

33.9

34.5

39.0

28.2

46.3

43.8

39.0

34.8

●

●

42.0

45.5

38.2

40.8

●

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

,., . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Place of residence

SMSA . . . . . . . . . . . . . . . . . . .

Central icy . . . . . . . . . . . . .

Noncentral city . . . . . . . . . . .

Outeide SMSA:

Nonfarm ., . . . . . . . . . . . . . .

,,, . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

,....., . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

,...,.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Farm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

SOURCE: National Center for Health Statistics: Prevalence ofselected chronic resptiatory conditions: United States, 1970. Vital arrd

Health Statistics.. Series 1O-NO. 84. DHEWPub. No. (HRA) 74-1511 .Health Resources Administration. Washington. U.S. Government

Printing Office, Sept. 1973.

33
Table8. Prevalence of emphysema reported onthe basis of physicians' diagnosis inhealth intewiew, bya~, family income, and place

of residence: United States, 1970

Family income and place of residence

Total .

Lessthan $3,000

$3,000-$4,999. .

$5,000-$6,989. .

$7,000-$9,999. .

$10,000-$14,999

$15,000 or more

SMSA . . . . . .. .

Central city .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Family income

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Place of residence

. .. . . . . . . . . . . . . . . ... .. . . . .. . . . . . . . . . ... . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Noncentral city . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

OutsideSMSA:

Nonfarm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Farm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Rate per 1,000 persons

6.6

14.5

12.0

7.5

5.1

3.4

3.4

5.4

6.1

4.9

8.8

7.7

1.0

●

●

●

●

●

☛

0.7

●

*

1.5

●

13.9

28.0

18.9

17.1

12.9

10.6

8.5

11.4

12.8

10.3

19.4

*

31.7

27.0

40.4

43.1

38.3

●

*

28.0

26.5

29.3

38.7

●

SOURCE: National Center for Health Statistics: Prevalence ofselected chronic respkatory conditions: United States, 1970. Vftaland

Health Statistics. Series 1O-NO. 84. DHEW Pub. No. (HRA) 74-1511 .Health Resources Administration. Washington. U.S. Government

PrintingOffice,Sept. 1973.

34
APPENDIXES

CONTENTS

I. Occupational Disease Reporting in California . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

Doctors’ Fmt Reportsand FmalDiagnoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

Information From Doctom’Reports. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

PotentialsforUseinStudies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

II. OccupationalDiseaseReportingandSurveyResuks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39

IIL Mortfllty Surveillance Using Coroner’s Reports . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

Background . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

Data Currently Available . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

Long-Term Objectives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

Present Status . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

Future Plans . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

Explanation of the Coroner’s Study Coding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

Daily Mortality Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

IV. ‘Ihe Continuous Work-History Sample . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.6

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45

Availability of Research Fiies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45

Six Available Files . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

I.imitation of CWHS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

Coverage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

Wages . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

Industry and Geographic Coding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47

Meeting of CWHS Users . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47

Data Development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

‘llm 1O-Percent Sample . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

Occupational Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

Place of Residence Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

FIGURE

I. Doctor’s First Report of Occupational Injury or Illness . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37

LIST OF APPENDIX TABLES

I. Number of medical conditions by occupational relationship among workers in small industries in

Oregon and Washington . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

II. ‘Ihesevencause-of.death codes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

35
APPENDIX I

OCCUPATIONAL DISEASE REPORTING IN CALIFORNIA

Esther Baginsky, Occupational Health Branch,

California State Department of Health

Under longstanding provisions of the California Worker’s Compensation Lawb all workincurred injuries and illnesses except first aid

cases are reportable to the State. By definition,

this includes any injury or disease arising out of

employment. It may result from one injury or

exposure or be the result of cumulative injury.

The law covers about 85 percent of the State’s

workers, currently more than 7.5 million people,

including farm workers and public agency employees. Excluded zmeself-employed persons and

those under Federal, maritime, or railroad compensation systems.

The physician is required to file his report,

Doctor’s First Report of Occupational Injury or

Illness (figure I), after the patient’s first visit. In

practice, he also forwards a copy to the insurance carrier as documentation of his medical

services. The carriers require a report from both

employer and physician for their claims procedures. The legal obligation to report applies to

the physician whether he performs on a fee-forservices basis or is salaried. In practice, however,

there is some underreporting by salaried physicians. Reports are not received from nurses in

b “Every employer, insurer, and physician or surgeon who attends any injured employee shall file with

the Division of Labor Statistics and Research a complete

report of every injury or occupational illness to each

employee arising out of or in the course of his

employment unless disability resulting from such injury

does not last through the day or does not require

medical service other than ordinary first aid treatment.”

(California Labor Code, Section 6409).

inplant medical services for care they give under

standing orders of a physician.

This system generates more than a million

physicians’ reports annually. About 40,000

reports of occupational illness for a selected list

of disease conditions are routed for review to

the California Department of Health. Included

are both lost workday and nonlost workday

cases.

Doctors’ First Reports and Final Diagnoses

Although the physician usually sees the

patient again, no further report to the State is

required. A survey in 1959 to determine agreement between the doctor’s first report and final

diagnosis showed that the final diagnosis generally agreed with the one given on the first report

and that the physician did not gain much more

information during patients’ revisits. This was

corroborated as recently as 1972 in a review of

medical records that showed that there was

seldom any additional information for the

doctor to base his diagnosis on other than

disease progression. All the information available to the physician regarding the worker’s

exposure is contained, in a majority of cases, in

the doctor’s first report.

How accurate is information given by physicians who are not specialists in occupational

medicine? Experienced occupational health

personnel concluded after an evaluation study

that in 8 or 9 out of 10 cases investigated the

reporting physician was correct when designating a case as probably occupational in origin.

36
DOCTOR’S FIRST REPORT STATE OF California

AGRICULTURE AND SERVICES AGENCY

OF DEPARTMENT OF INDUSTRIAL RELATIONS

OCCUPATIONAL INJURY OR ILLNESS

DIVISION OF LABOR STATISTICS AND RESEARCH

P. O. Box965,SanFrancisco,Calif.94101

Immediately after first examination mail one copy directly to the Division of Labor Statistics and Research. Failure to file a

report with the Division is a misdemeanor. (Labor Code Section 6413.5) Answer all questions fully.

W A, INSmNcE cmR .....................................................J...................................................................................................... .......

L EMPLOYER .... ... .. .... . ., ..... . . . . .. . ..... .. . ............................................................. .....

2. Address ‘&?#j . . . .. . . . . . . . .. . . . . . . . . . . . . .. . . . .. . . . . . . . . . . . . .. . . . . . .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . .. .. . . . . . . . . . . . . .. . . . . . . . . . . . .... ..................... .. .....

3. Business ‘%~$~% Ihml,tl,uiymll- Illml, Clou, etc.) .. .................. .......... ..... . ....................................... .......... .................................

4.

5<

6,

7.

8.

9.

10, Name oher doctors who treated employee for this tijV ......................~... .....~.... ....... . ... .... ... .. .........................

EMPLOYEE (Wmfrs.1,.ame, h$t mm) middle -------------------------------------- . .. . . . . . . . . .. . . . . . .. . . . . .. .. . . .. . .. . . . .Sot. Sec. No.......................................

Address ‘~~~j ....................................................................................................................................................................

Omupation ......................................................................................... ................Age ........... ....................Sex.........._.........

Date injured ............................. .._...................Hour... . . .....M. Date last worked ..... . . ....... ............................ .......

Injured at ‘$’l&i$j....................................................................................................................Coun~ ........................ ....

Date of vour first examtiation ......................Hour ................M. Who engaged your servi&s? ......... .. ... ................

11. ACCIDENT OR EXPOSURE: Did employee notify employer of this inju~? . ... Employee’s statement

of cause of injury or illness:

12, NATURE AND EXTENT OF INJURY OR DISEASE (Include all objective findings, subjective complaints, and

diagnoses. If occupational disesse stste date of onset, occupational history, and exposures. )

13. X-rays: By whom taken? (stat. ii non.). ... . .... ............................................................ ..... ................................. .. .. ....

Findings:

14, Treatment:

(OS&, home 15. Kind of case ., ho,pi~.l) . If hospitalized, date... Estimated stay .... .. ....... ... ...

Name and address of hos ital ............. ............................................................................................................................

16. Further treatment (Esrim.tlfmu..ey

and duration) - ---------------------------------------------------------- . . . . .. . . . .----------------------------------------------------------

17. Estimated period of disability for: Regular work .........................................MdMd work-................................ ....

IS. Describe any permanent disability or disfigurement expected (state;fnone)...... ...................................................... ..

19. If death ensued, give date

20. REMARKS (Noteanypre-existinginjuriesor diseases, needfor special examinationorlaboratorytes@otherpertinentirsfomration.

[

FERSONAL

Name . . . ...................... ... ... ...........Degree... .. . ~\G#~l~~~

(TYPOor SUM) 1.. ..

no not write

ir! this ml.cm

Date of report ......... ... .... . ............ Address ‘&#... ....... .. .................. ...................................... ................... .............................. ....

FORM S021 [REV, 1) Uae reoeree aide if more spaoe required n 0s,

Figure 1. Doctor’s First Report of Occupational Injury or Illness

37
Information From Doctors’ Reports

The doctor’s report identifies the worker,

employer, insurance carrier, and physician.

While the employee’s social security number is

supplied on three-fourths of the reports, occupation is often missing or only vaguely described.

Age and sex are almost always reported.

The employee’s statement concerning the

exposure and symptoms and the physician’s

findings and diagnoses are the basis for regularly

produced California statistics on occupational

disease. Certain limitations should be noted,

however, in the detail contained in physicians’

reports. Ten percent of alI reports have no

“hazard” classification and are coded “unknown.” In addition about 30 percent classify

exposure hazards in some “other and unspecified” category (e.g., gas, dust, etc.) or as

chemically unspecified materials identified by

use (e.g., solvent, paint, cleaning compound,

agricultural spray, etc.).

One-half of all the reports reviewed in 1973c

described skin diseases or disorders, such as

dermatitis, chemical burns, and inflammations.

Another 30 percent listed eye conditions,

mainly chemical conjunctivitis. Ten percent

showed respiratory conditions and systemic effects of toxic materials. The remaining reports

included disorders due to physical agents, infective and parasitic diseases, heart conditions,

neoplasms, and other infrequently reported conditions.

Chronic or latent diseases are underreported

in the California reporting system, as they are in

most other occupational injury and illness reporting systems. In 1973, for instance, only 162

cases of noise-induced hearing loss were reported; on the other hand, studies of operating

engineers and drillers in construction have

shown that more hearing loss exists in these

groups than is reported for all workers. There

were 13 reports of pneumoconiosis, about the

same as in previous years, yet 80 death certificates were filed in 1973 with mention of

pneumoconiosis. Doctors’ reports of neoplasms,

benign or malignant, numbered 25.

Files of doctors’ reports are maintained for 3

years. For a few conditions they nave been

retained for as long as 10 years. Among the

selected cases are poisoning by heavy metals,

certain gases, and pesticides. Coded data for all

reports are also stored on magnetic tape for data

retrieval and statistical use; however, the only

identification is the name of the employer.

Potentials for Use in Studies

The recognition and reporting of workincurred illness depends on what the patient and

physician recognize as being related to occupation based on past experience, specialized training, and alertness to occupational health

hazards. There are limited opportunities, therefore, to anticipate and recognize new problems

on reports filed by physicians.

The most fruitful uses of doctors’ reports of

occupational disease would appear to be in

providing background to initiate studies. As

shown below, the reports could be used to:

Provide clues to initiate industry studies

with specific health exposure problems (e.g.,

eIectroplating, woodworking, etc.).

Provide followup of workers who have reported certain occupational health problems

already reco~ized (e.g., lead poisoning,

chlorinated hydrocarbon solvent exposures,

etc.) in order to study possible long-term

effects. For workers selected in such a

manner, Iinkup with other sets of data might

be useful.

Provide a basis for setting priorities for

study.

Provide information useful in setting occupational health standards.

categories of illness reviewed by the Occupational

Health Section, California Depzwtment of Health, differ

in somerespectsfrom those defined in Federal and State

Occupational Safety and Health recordkeeping regulations.
APPENDIX II

OCCUPATIONAL DISEASE REPORTING AND SURVEY RESULTS

Esther Baginsky, Occupational Health Branch,

California State Department of Health

From July to December 1971, as part of a

survey of occupational illness in certain establishments in California funded by the National

Institute for Occupational Safety and Health, a

comparison was made of nonfatal occupational

illnesses reported in the survey with those

reported on the Doctor’s First Report of Occupational Injury or Illness. In general, the ratio of

doctors’ reports to NIOSH survey cases was

0.74, with a higher ratio for cases with a lost

workday (0.84) than for cases with no workday

loss (0.71).

A survey involving interview and examination of workers among small industries in

Oregon and Washington was reported by

Discher, Kleinman, and Foster.z

The study had two goals: (1) to determine

the utility of procedures designed for finding

occupational disease in a cross-sectional survey,

and (2) to ascertain how much new data would

be generated by this method.

Some of the findings were:

Over 1,100 medical conditions were found

among 908 participants: probable occupatier-ud, 31 percent; probabIe nonoccupational, 45 percent; doubtful occupational or

can’t evaluate, 14 percent; and suggestive

history, 10 percent.

Of 346 cases of probable occupational

disease, hearing loss was most frequent, 28

percent; then skin, 18; lower respiratory

conditions, 14; toxic and low-grade toxic

effects and nonsymptomatic conditions

(mainly elevated blood leads), 14; upper

respiratory conditions, 11 percent; and eye

conditions, 9 percent. Anemia, diseases of

the musculoskeletal and connective tissues

and other conditions accounted for the

remaining 6 percent.

Of the 908 workers participating in the

medical survey, 258 workers were found

with 346 cases of probable occupational

disease, giving a prevalence rate of 28.4 per

100 workers. Occupational exposures were

determined for all workers in the survey.

Those known to have been ‘exposed to

poorly controlled hazards had a higher prevalence rate (39.0).

The survey morbidity data were checked for

duplication with records of compensation

claims and injury and illness records employers are now required to keep under

OSHA (Employer’s Log). Of 451 reports of ,

occupational disease, 89 percent were

found on the survey only; 2 percent on the

Employer’s Log; and 3 percent on compensation claims only; 6 percent “were duplications.

A nationwide survey is recommended, based

on techniques developed in this study, for an

estimate, not available elsewhere, of the extent

and kinds of occupational disease. The results

would help delineate problem areas, ascertain

39
Table 1. Medical conditions by occupational retationshirJ amona workers in small industries in Oregon and Washington

Medical condition 1

Total . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Anemia andotherdiseasasofblood . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Conjunctivitis and otherconditionsof theeye. . . . . . . . . . . . . . . . . . . . . .

Refractiveerrors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Hearingloss,mild . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Hearingloss,moderate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Hearingloss,advanced . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Hearingloss,possiblethrashold. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Heartdisease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Otherdiseasesofcirculatorysystem . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Respiratory conditions, excluding upper . . . . . . . . . . . . . . . . . . . . . . . . .

Upperraspiratory conditions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Skin conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Disaasa ofmusculoskeletal and connective tissues . . . . . . . . . . . . . . . . . . .

Symptomsand illdefinedconditions . . . . . . . . . . . . . . . . . . . . . . . . . . .

Nonsymptomaticconditions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Toxicandotheradverseeffects, . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Lowgradetoxiceffects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Otherconditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Total

1,116

49

74

84

86

32

4

16

138

14

3

289

73

128

28

17

27

23

14

17

tional

disaase2

346

7

31

0

68

26

2

0

1

0

0

49

38

64

9

1

27

9

13

1

Can’t be

evaluated3

and

doubtfu14

151

21

1

1

12

4

2

16

0

1

0

76

2

4

2

6

0

1

1

1

suggestive

I istory 5

113

1

24

0

0

0

0

0

0

0

0

11

21

35

7

1

0

13

0

0

Probable

nontional

disease6

506

20

18

83

6

2

0

0

137

13

3

153

12

25

10

9

0

0

0

15

lDo~snot include employees who took hearing tests onlY.

2Manifestation~ ofdisease areconsistent tith those knowrr to result from excessive exposure toagiven injurious agent; this injurious

age t is present inthepatient’s working environment and significant contact in course of usurdduties is likely.

2 An association between disease and occupational factors has never been clearly established; e.g., c~tiov~cular disease, respiratory

infe tions, mental andpsychoneurotic epkodes.

i

(1) Manifestations of disease are not entirely consistent with those known to result from excessive exposure to an injurious agent or

(2) &anifestations of illness are consistent with those known but no significant contact with rsfleged injurious agent can be established.

Manifestations of disease eagiven inhiatory are consistent with those knomtoresult from excessive exposme toa given injurious

age t;thisexposure isor has taken place; there isnoobjective evidence of disease atthe time of themedicsd examination. %Manifestations of disease but no relationship to occupational exposures.

adequacy of standards, and might provide new

insights into the relationship of occupational

exposures and diseases.

Table I shows the definitions of “Probable

occupational disease,” etc., andthe frequency of

relevant categories of medical conditions according to the likelihood of an

relationship.

occupational

o

40

0 0
APPENDIX Ill

MORTALITY SURVEILLANCE USING CORONER’S REPORTS

Margaret Deane, Epidemiological Studies Laboratory,

California State Department of Health “

Background

Since the early 1950’s the California Health

Department has been interested in providing to

the general community a warning of excess

mortality or morbidity through a mechanism

which would respond rapidly to significant

changes. Such a system meets the definition of

surveillance, which implies continuing measurement and examination of some index in a

manner allowing prompt action to alter the

forces causing departures from expected values.

In 1954, the department began operating a

mortality surveillance system using weekly reports of deaths and admissions to hospitals from

about 100 nursing homes in the Los Angeles

area.

The study was based on the idea that the

nursing home population largely represented old

and chronically ill people who would be expected to be relatively sensitive to the effect of

the environment. When initiated, it was planned

as a system which, on a few hours’ notice, would

alert the community to the occurrence of

excessive mortality. Although the regular weekly

reports were received by mail, during periods of

high air pollution, data were obtained by telephone with a lag time of only a few hours.

The nursing home study was discontinued in

1967 for two reasons. First, many of the homes

had acquired air conditioning so that the patients were no longer exposed to environmental

conditions characteristic of those impinging on

the general noninstitutional population. Second,

the possibility arose of using mortality data

from the Los Angeles Coroner’s Office, which

had indications of being a more manageable and

effective source of data.

Data Currently Available

Since 1968, the Los Angeles Coroner’s Office has sent weekly reports of all cases recorded

during the preceding week. The reports are

based on the daily log, which is the most quickly

available source of information and which includes name, age, sex, date (or presumed date)

of death,.and an indication of whether the death

was presumptively classified as “suicide,”

“homicide,” “motor vehicle accident,” “other

accident ,“ or “due to natural causes.” Data are

edited and transferred to computer tape for

subsequent processing.

Coroner’s reports have several advantages

over general daily mortality for use in a surveillance system. First, they are available on a

current basis, while data based on total vital

statistics are not. Furthermore, since the reports

originate in coroners’ offices rather than in

numerous hospitals and other institutions, it

should be relatively easy to establish a system of

collection and transmission that would provide

data even faster than that presently available,

reducing the lag time from between 1 and 2

weeks to between 1 and 2 days. This might be

done by entering the data through a remote

computer terminal located in the coroner’s

office. Second, since coroner’s cases represent a

selected group of deaths, that is, those resulting

from violence or suicide, those of individuals not

41
in attendance by a physician, those in which the

cause of death is unknown, and those following

an injury or accident, they may be more

sensitive than general mortality to environmental causes and effects of drugs and pesticides. For example, rates for accidents and other

sudden deaths may be more affected by air

pollution and weather; and homicides, suicides,

and poisoning may be more closely related to

drug use, especially among young adults. By

obtaining additional medical data following

autopsy or by record linkage to obtain cause-ofdeath information from death certificates, it

should also be possible to examine some specific

causes of death that are particularly apt to be

related to environmental factors. These could

include myocardial infarctions, deaths of early

infancy, childhood cancer, anemia, leukemia,

and blood dyscrasia.

About 40 coroner’s cases per day are reported from Los Angeles County, or between

14,000 and 15,000 per year. Thus for the 5-year

period 1968-72, we have about 75,000 records

available for analysis. Coroners’ cases should

therefore be applicable as a surveillance index

for other large metropolitan areas, and can

provide guidance for evaluating medical service

needs.

Long-Term Objectives

One objective of mortality surveillance is to

develop a system that can be used to detect

departures from “expected” numbers of deaths

to alert officials to seek the cause, whether it be

an increase in communicable disease, effects of

some social factors such as alcohol or drugs, or

an effect of such environmental factors as

pollution or weather. To be effective, such a

system must use methods of collection, transmission, updating, editing, and analysis that give

results promptly enough so that effective action

can be taken to alter the force of mortality.

Another aim is to carry out analyses designed to investigate the relationship between

dailj mortality as reflected in coroner’s reports

and causative factors that are amenable to

controI; for example, air or water pollution,

weather, pesticides, drug abuse, prenatal effects.

These analyses would have two results. First, to

support hypothesis that such relationships do, in

fact, exist, and second, to provide a basis for

establishing expected values based on past experience.

Present Status

Data for 1968-74 have been edited and are

available on computer tape in a format suitable

for analysis. Several models are being tested to

establish expected values based on these 5 years

of data. The years are treated as replicates of a

52-week period and Fourier analysis is being

used to fit curves with up to nine harmonics.

Departure of weekly values for 1973 from

expected values predicted from these curves will

then be examined in relationship to statistical

significance and coincidence with environmental

factors such as elevated levels of air pollution

and ambient temperature, taking into account

also the effect of epidemics. Alternatively, expected wdues have been calculated using moving

averages of the 5-year means for each week.

Future Plans

Depending upon the availability of resources, further work will be done in developing

and testing the predictive models and in examining departures of current data from predicted values. These also may include multiple

regression models including pollution levels,

humidity, time of year, trend, and various

functions of these including rapidity of change

over time. The use of discriminative analysis is

aIso being considered. Cu-sum methods may be

used to test for significant departures from

predicted values.

Explanation of the Coroner’s Study Coding

Cause of death is the only item to be

coded. However, there are other items on the

form that must be edited.

1. Age is probably the most frequent

problem to arise. As the age of infants is often

given in months, this should be the first item

coded on the form since we wish to convert age

into years in a three-column field.

42
All ages underl year should becoded OOO. Table Il. Theseven cause-ofdeath codes

All ages between 12 months and 23 months

should be coded 001.

Any age unknown should be coded 999.

Stillborn should be lined out completely

and not coded.

2. Frequently, entries will appear that are

not coroners’ cases. These can be determined by

the letters “NCC” usually found in the column

labeled “Disposition.” These cases should also

be lined out and not coded.

3. Usually, there will appear on the green

sheet a list of numbers or items labeled “Holdovers.” These holdovers should be lined out and

not coded. They will appear in a later report.

4. There are seven cause-of-death codes (see

table II). The cause of death should be coded in

red pencil just to the right of the cause.

The name of the doctor is no longer being

coded. On the white sheet, the doctor’s name

appears in the extreme right-hand column labeled “Disposition.” On the green sheet, the

doctor’s name appears in the left-hand column

above the case numbers assigned to the doctor.

A list of code numbers is attached. The code

number should always be coded on the extreme

left margin of both forms. If a doctor’s name is

not on the list of code numbers, add the name

to the list and assign it the next number.

Surveillance of Daily Coroner% Reports

Col. Explanation

1-2 Year of report

3-7 Case number

8-11 Date of death

8-9 Month

10-11 Day

12-16 Time of death

12-13 Hour

14-15 Minute

16 AM: I; PM: 2; UNK: 9

If 2 dates appear here, the first date is the

day of death; the second date is the day the

death was reported to the coroner’s office. In

coding, the second date can be ignored.

Code I

Causa

1. Motor vehicle accidents . .

2. Nonmotor vehicle accidents . . . . . . . . . . . .

3. Suicide . . . . . . . . . . . . .

4. Homicide . . . . . . . . . . .

5. Naturall . . . . . . . . . . . .

6. Possibly naturall . . . . . .

7. Undetermined . . . . . . . .

Collisions involving motor vehicles (cars, buses, trucks,

motorcycles, tractors)

Airplanes, trains, industrial

accidents, fires, and “accident,” “possible accident,”

“accident?”

“Suicide:’ “possible suicide;’

‘%uicide?”

“Homicide#” “possible homicide,” “homicide?”

“Natural”

“Possibly natural,” “apparently

natural, “ “natural?”

“Undetermined,” or a combination of any two of the

above causes; e.g., “natural?-

accident?”

lThere j~ no di~cernjble difference between number 5 and

number 6.

17-36

37-51

52

53-55

56

57-60

57-58

59-60

61-65

61-62

63-64

65

66

67-68

69-70

71

Last name

First name

Middle initial

Age (1-12 mos:OOO; 13-23 mos: 001)

B1ank

Date brought in (if different from

first date)

Month

Day

Time brought in

Hour

Minute

AM: l; PM: 2; UNK:9

Cause of death

SO (death signed out) or A (autopsy

performed)

Doctor

Outside: 1; Inside: 2

Daily Mortality Data

In large populations, the frequency of deaths

is such that variations in daily mortality can be

used aa a sensitive index of health effects which

are influenced by changes in environmental

43
factors. In New York City, for example, daily approach should be exploited in other large

mortality is sensitive to moderate fluctuations of cities for similar purposes. These investigations

temperature, and when suitable controls are have been handicapped by the NCHS decision in

made for temperature, season of year and other 1967 to discontinue punching the day of death

factors, the’ daily mortality varies with atmos- on death records. This information must now be

pheric sulfur dioxide levels. This valuable obtained less efficiently from local sources.

000

,’,

. . . . . . .
APPENDIX IV

THE CONTINUOUS WORK-HISTORY SAMPLEd

David A. Hirschberg,e Special Assistant,

Liaison for Outside Users,

Office of Research and Statistics,

Social Securs”ty Administration

INTRODUCTION

In administering the social security system,

an unprecedented volume of economic and

demographic data is generated. Much of this

basic information is summarized in the monthly

Social Security Bulletin, and its Annual Statistical Supplement; and in special releases and

reports.

Because the basic administrative records

have great value for economic and social research, it is the general policy of the Social

Security Administration (SSA) to make its data

resources available for this purpose. Such research must meet two conditions: it must

provide for safeguarding the confidentiality of

information for individuals, firms and reporting

units; and it must be feasible without impairing

the administration of the social security program.

Our publication, Some Statistical Research

Resources Available at the Social Security Administration, provides a detailed description of

the available data files, the procedures used in

their compilation, and how they may be obtained. The overall research program of the

Social Security Administration is detailed in the

‘This paper was developed for presentation at the

August 1974 American Statistical Association meeting.

ePosition at time paper was prepared. ~. Hirschberg

is currently with the U.S. Department of Labor.

annual Work Pl&-Iof the Office of Research and

Statistics.

AVAILABILITY OF RESEARCH FILES

Much of the analytical data drawn from our

administrative records are most conveniently

handled by the use of samples. In order to

provide, at modest cost, outside users with a

general resqarch file, SSA makes available an

Annual One-Percent Continuous Work-History

Sample. The nature of this data file may best be

understood by seeing how the various sources of

data come together.

When a person applies for a social secunt y

number he provides data on his sex, race, and

date of birth, enabling us to maintain a file of

individuals by social security number (SSN),

sex, race, and age. When an employer requests

an employer identification number (EIN) he

provides data on his geographic location and

industry activity, enabling us to maintain a file “

of employers by EIN coded to State and county,

and industry (4-digit SICf in manufacturing and

3-digit SIC in nonmanufactunng). Each quarter,

covered employers report the wages of their

employees up to the taxable limit. (Agricultural

and self-employed data are reported annually.)

By matching the earnings data first to the SSN

file, and then to the EIN file, we obtain for each

job quarter, data on sex, race, and age, State and

count y, industry, and wages.

fStandard industrial classification.

45
Most

sampling

inclusion

importantly, the selection of a fixed

pattern of social security numbers for

each year permits the establishment of

a work-history file- for tracing employment,

migration, and earnings status of all those who

worked in covered industries and for determining their socioeconomic characteristics from

1957 to date. As new workers enter the workforce, those with the specified digits enter the

annual sample; as others drop out of the covered

workforce those with the specified digits no

longer appear.

More recently, claims data have been introduced into the file. These, of course, are

obtained from the application for benefits and

the Master Beneficiary Record, a comprehensive

record for all benefits in force.

Six Available Files

Six files, all of which contain data for sex,

race and age, are available to outside users. So

that the files may be utilized for Iongitudimd

studies, and the confidentiality of individuals

and firms be maintained, the employee and

employer identification is included in scrambled

form.

One-percent annual employee-employer

@e.-This includes wage and salary employment

report ed in the reference year, with one record

for each employee-employer combination. Basic

data elements include annual and quarterly

taxable wages, total estimated wages, State and

county, industry, and coverage group (for

example, farm, military, and household). This

file becomes available approximately 2 years

following the year of reference. Currently the

file is available for each year from 1957 to 1971.

One-percent j?rst-quarter employeeemployer file. —This file contains the same data

elements as the annual file, except that it

becomes available about 15 months after the

quarter of reference. Because an effort is made

to obtain the file as quickly as possible, late

reports are excluded and coding problems which

may exist are not resolved. Excluded are agriculture and self-employment data, which are

reported on an annual basis.

One-percent sample longitudinal employeeemployer abta (LEED) file. —The basic data

elements are the same as in the annual file,

except that the records are skeletonized, arc

currently available from 1957 to 19.70, and are

sequenced so that all records associated with an

employee appear together.

One+ercent sample annual sel’employed

file. -This file includes the same basic data

elements as the employer-employee files, but

covers net and taxable earnings for those who

are self-employed, The basic source is the IRS

Schedule SE. The earliest date of availability is

1960.

One+ercent 1937-to-date continuous workhistory sample (CWHS). —This file provides

various data indications from 1937 including

yea’s employed, first and last years employed,

pattern of quarters employed for the last two

years, number and quarters of coverage beginning with 1937, patterns of coverage beginning

in 1957, farm or nonfarm wage or selfemployment indicators, taxable and selfemployed earnings each year beginning in 1951,

and insurance status and benefit information.

One-tenth percent 193 7-to-date continuous

work-history sample (CWHS) file. –This file

provides the same data as the one-percent

CWHS, but includes a greater level of detailed

earnings information beginning in 1937. There is

no geographic or industrial detail.

LIMITATION OF CWHS

When administrative data are used for analytical purposes, the researcher must be aware

of some problems and limitations. These occur

because the, entire labor force is not covered and

the employer reports only wages up to the

taxable maximum. Moreover there are problems

of timing, improving the geographic and industry coding, and of sampling and nonsampling

errors in utilizing the data.

Coverage

No major changes in the coverage provisions

of the social security system have taken place

since 1954, Currently the sample covers well

over 90 percent of workers in paid employment.

Two types of Old-Age, Survivors, Disability,

Hospital Insurance coverage exist: mandatory

and elective.

employees in

On a mandatory basis are all

nonfarm industries (except rail46
road workers), most farm and domestic employees who meet minimum earnings provisions,

and Federal employees not covered by the

Federal retirement system. Groups covered on

an elective basis are ministers, nonprofit establishments, and State and local government

workers. All self-employment is covered if earningsexceed $400 per year.

Essentially for those with more than just

marginal earnings, excluded are 3 million Federal workers, 3 of the 10 million State and local

government workers, and a small number of

nonprofit employees, since most elect coverage.

Wages

Several problems arise when administrative

wage data are used for analytical purposes. The

major limitation is that the employer reports for

each worker the wages to the taxable limit. The

taxable limit has risen steadily since 1957 when

it was $4,200; currently it is $13,200. Because

nonfarm wage data are reported by quarter, an

estimate of total wages is possible. This procedure estimates the total wage by substituting the

last full quarter wage for the quarter in which

the taxable limit was reached, and for each

subsequent quarter.

For those workers who reached the taxable

limit in the first quarter, separate annual estimates for males and females are prepared for

each year based on the Pareto method.

Industry and Geographic Coding

As mentioned previously, industry and geographic coding data are obtained when a firm

applies for an EIN. On the same form is the

question asking if this is a multiestablishment

firm. If the answer is “Yes,” the firm is.asked to

participate in our Establishment Reporting Plan

covering multiestablishment firms. Ideally, we

would like to obtain from each firm an individual report for each establishment. However,

reporting by establishment is voluntary, and

because of other priorities, only a limited

number of technicians are assigned to deal with

establishment reporting problems. Simply put,

the problem is one of editing, reviewing, and

correcting, if necessary, several million firm

reports

studies

received each quarter. We are planning

to determine the effect of the reporting

difficulty and how its impact can be minimized.

The file does contain internal coding, each

record indicating how the industry and geographic assignment has been made. This is a

great help in editing the file so that spurious

changes can be identified; the nature of the edits

depend upon the research undertaken.

Although researchers using the file should be

aware of these limitations, the CWHS is still a

powerful analytical tool. It permits extensive

disaggregation by sex, race, age, industry, geography, workforce participation; and earnings

levels. It follows the same individual workers

over time so that quarter-to-quarter or year-toyear changes for specific individuals can be

observed. Most important, as Nancy and Richard

Ruggless 9 have pointed out, it can be successfully disaggregated to show the anatomy of the

total wage bill as it relates to the national

economy.

When used to examine migration, the fiIe

provides for the development of area data on

gross flows, as compared with net flows, because

the net may be an average that masks important

characteristics of two very different gross flows.

Cross-sectionaI data on earnings and mobility status can at best be only partly informative;

generally they are misleading. For example,

workers who move from one area ,to another

(migrants) earn less than nonmigrants. However,

migrants increase their earnings at a faster rate

but start from a lower base. If we examine

census data, the nonmigrants appear to be the

higher paid group, and some economists have

suggested, therefore, that mobility does not

improve the economic status of migrants.

MEETING OF CWHS USERS

A CWHS users conference is held each year.

Invitations are extended to anyone interested in

the problems of handling the data files, to those

who wish to report on recent research findings,

and to those involved in preparing the file in

SSA. These meetings over the last several years

have provided users of the data with a better

understanding of the work currently under way,

and have enabled the producers to discuss .

several of the new developments

file, and methods to improve it.

relating to the

47
DATADEVELOPM ENT

The 10-Percent Sample

The one-percent CWHS currently available

has important limitations when used for

studying small standard metropolitan statistical

areas (SMSA’S) and rural areas. The initial

impetus for the development of a ten-percent

sample file came from OMB (Office of Manpower and Budgeting) as a result of urgent needs

for intercensal population estimates for revenue

sharing and other programs, and because of the

decision not to conduct a mid-decade census. At

present, the Department of Housing and Urban

Affairs is providing the bulk of the funding and

other Federal agencies make significant contributions.

The data base for this file will be similar to

the first quarter files described earlier, and will

include those working in the first quarters of

1971 and 1973. In the United States during the

first quarter of 1971, approximately 73 million

workers held 80 miIlion jobs. Therefore, the

1971 file will contain records for 7.3 million

workers and 8.0 million jo’bs. The 1973 file will

be approximately 6 percent larger.

For each year, the records will be summarized so that the industry and place of work is

available for the major job. The file will be

merged, indicating for each individual the sex,

race, age, if his employer changed, and (for 1971

and 1973) geography, industry, and wages. The

file will be sorted so that tabulations by State

and county for both years will be available at

modest cost.

The ten-percent sample would constitute a

significant asset for regional ~alysis. No other

source of data could provide insight into the

structure of a 10cal area labor force, so that

employment distributions by sex, race, age,

wages and wage changes, workf orce participation, industry, and regional migration patterns

could be analyzed systematically.

Occupational Data

In addition, a detailed proposal has been

prepared to test the feasibility of adding occupation as a standard data item to the CWHS. It is

contingent on Intemzd Revenue Service (IRS)

cooperation. The approach is to use the IRS

1040 occupation information supplemented by

followups when necessary with employees, and/

or employers. The proposal is under serious

consideration with other statistical agencies and

is pkmned in two stages. The first stage will be a

feasibility and quality analysis based on a sample

of 15,000 CWHS wage earners. It will be

designed to examine the cost and operational

feasibility of this approach and to explore issues

of quality-in particular, the extent to which

occupation entries on the IRS 1040 can be used

for classification beyond the major group level.

If the pilot project indicates that this

approach to the collection of occupational data

appears feasible and produces data of acceptable

quality, the project would go into a second

phase, expanded to another 60,000 workers, or

a one-in-a-thousand sample.

Place of Residence Data

In another project, a modified version of the

Census Bureau’s address reference file is being

used to automatically assign geographic codes to

the 1972 CWHS. This operation will provide for

pIace of work and pIace of residence comparisons, and also facilitate the editing of the

file.

CONCLUSION

Ideally a research file of this scope should

contain additional information. Occupation and

place of residence have already been mentioned.

Timeliness of the data has been improved with

the availability of first quarter files. In terms of

coverage, efforts will be explored to provide

data for the noncovered portion of the CWHS.

There is a need to incorporate data from the

Railroad Retirement System and the Civil

Service Commission. (In addition, educational

attainment, hours of work, marital status, unemployment, and noncovered wages are other

important variables to consider.)

In conclusion, the operation of the Social

Security System produces a vast and unique body

of longitudinal data on earnings, and on retirement and disability claims and benefits for

persons classified by age, race, and sex. It has

been our policy to make the data available to

48
social scientists. Over the past year, admin- grateful. In undertaking these projects, we will

istrativc and research agencies of government always be careful to safeguard and protect the

have been extremely helpful in moving some of confidentiality of information relating to indithesc research efforts forward and we are viduals.

000

I

17139 *U. S. CQVERN42NI PRINTING OFFICE: 1979 281-259/22

49
1, ..ll,_.

VITAL AND HEALTH STATISTICS Series

Series 1. Programs and Collection Procedures. –Reports which describe the general programs of’ the National

Center for Health Statistics and its offices and divisions and data collection methods used and include

definitions and other material necessary for understanding the data.

Series 2. Data Evaluation and Methods Research. –Studies of new statistical methodology including experimental tests of new survey methods, studies of vital statistics collection methods, new analytical

techniques, objective evaluations of reliability of collected data, and contributions to statistical theory.

Series 3, Analytical Studies. –Reports presenting analytical or interpretive studies based on vital and health

statistics, carrying the analysis further than the expository types of reports in the other series.

Series 4. Documents and Committee Reports. – Final reports of major committees concerned with vital and

heafth statistics and documents such as recommended model vital registration laws and revised birth

and death certificates.

Series 10. Data From the Health Interview Suruey. –Statistics on illness, accidental injuries, disability, use of

hospital, medical, dental, and other services, and other health-related topics, all based on data collected

in a continuing national household interview survey.

Seric\ 11. Data From the Health Examination Survey and the Health and Nutrition Examination Survey .–Data

from direct examination, testing, and measurement of national samples of the civilian noninstitutionalized population provide the basis for two types of reports: (1) estimates of the medically defined

prevalence of specific diseases in the United States and the distributions of the population with respect

to physical, physiological, and psychological characteristics and (2) analysis of relationships among the

various measurements without reference to an explicit finite universe of persons.

Series 12. Data Fro m the institutionalized Population Survey s.–Discontinued effective 1975. Future reports from

these susveys will be in Series 13.

Series 13. Data on Health Resources Utilization. –Statistics on the utilization of health manpower and facilities

providing long-term care, ambulatory care, hospital care, and family planning services.

Series 14. Data on Health Resources: Manpower and Facilities. –Statistics on the numbers, geographic distribution, and characteristics of health resources including physicians, dentists, nurses, other health

occupations, hospitals, nursing homes, and outpatient facilities.

Series 20. Data on Mortality. –Various statistics on mortality other than as included in regular annual or monthly

reports. Special analyses by cause of death, age, and other demographic variables; geographic and time

series analyses; and statistics on characteristics of deaths not available from the vit21 records based on

sample surveys of those records.

Series 21. Data on Na8a[ity, Marriage,’ and Divorce. –Various statistics on natality, marriage, and divorce other

than as included in regular annuaf or monthly reports. Special analyses by demographic variables;

geographic and time series analyses; studies of fertility; and statistics on characteristics of births not

available from the vital records based on sample surveys of those records.

Series 22. Data From the National Mortality and Natality Survey s.–Discontinued effective 1975. Future reports

from these sample surveys based on vital records will be included in Series 20 and 21, respectively.

Series 23. Data From the National Survey of Family Growth. – Statistics on fertility, family formation and dissohstion, family planning, and related maternal and infant health topics derived from a biennial survey

of a nationwide probability sample of ever-married women 15-44 years of age.

For a list of titles of reports published in these series, write to: Scientific and Technical Information Branch

National Center for Health Statistics

Public Health Service

Hyattsville, Md. 20782

~-” -1 -———— -——
NCHS

POSTAGE ANO FEES PAIO

U.S DEPARTMENT OFH E.W

HEW 396

0*-_ Ii