EPA-600/1-77-019
April 1977
Environmental Health Effects Research Series
OCCUPATIONAL AND ENVIRONMENTAL PESTICIDE
STUDY IN SOUTH FLORIDA
Health Effects Research Laboratory
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina 27711
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RESEARCH REPORTING SERIES
Research reports of the Office of Research and Development, U.S. Environmental
Protection Agency, have been grouped into nine series. These nine broad cate-
gories were established to facilitate further development and application of en-
vironmental technology. Elimination of traditional grouping was consciously
planned to foster technology transfer and a maximum interface in related fields.
The nine series are:
1. Environmental Health Effects Research
2. Environmental Protection Technology
3. Ecological Research
4. Environmental Monitoring
5. Socioeconomic Environmental Studies
6. Scientific and Technical Assessment Reports (STAR)
7. Interagency Energy-Environment Research and Development
8. "Special" Reports
9. Miscellaneous Reports
This report has been assigned to the ENVIRONMENTAL HEALTH EFFECTS RE-
SEARCH series. This series describes projects and studies relating to the toler-
ances of man for unhealthful substances or conditions. This work is generally
assessed from a medical viewpoint, including physiological or psychological
studies. In addition to toxicology and other medical specialities, study areas in-
clude biomedical instrumentation and health research techniques utilizing ani-
mals — but always with intended application to human health measures.
This document is available to the public through the National Technical Informa-
tion Service, Springfield, Virginia 22161.
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EPA-600/1-77-019
April 1977
OCCUPATIONAL AND ENVIRONMENTAL PESTICIDE EXPOSURE STUDY IN SOUTH FLORIDA
By
Dr. John E. Davies
University of Miami School of Medicine
1600 N. W. 10th Avenue
Miami, Florida 33152
Contract No. 68-02-1760
Project Officer
Dr. Thomas M. Scotti
Environmental Toxicology Division
Health Effects Research Laboratory
Research Triangle Park, N.C. 27711
U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF RESEARCH AND DEVELOPMENT
HEALTH EFFECTS RESEARCH LABORATORY
RESEARCH TRIANGLE PARK, N.C. 27711
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June IS, 1973
EP.SATA
SUBJECT: EPA-600/1-77-019
April 1977
TITLE: OCCLWriOtlW. JWD ENUIROMEKTAL PESTICIDE STTOY IN
SOUTH FLORIDA
The following corrections should te made to the above report;
i. Page 17 - first paragraph, lines 7 and &: 3,5,6-Tridilorophenol
(3.5,5-TCPJ Sho'jld be 3.5 ,6-trictiloropyrldino]
(3,5,6-TC J
t. Page TB - Table 4 C: 3.5,6-TCP (after "C'nTorpyrlfos") stiould be
3,5,6-TC Pjrldinal
3, Page 48 - Table 14. coljnrn heading 2,3.5-TCP sdoiiTd 6e 3,5,6-TC
PyHdinol
4. Page fa - Appendix A: 3,5,5-TCP (under "Phenols") should be
3,5,6-TC Pyridlnol
5. Page 63 - Attached is a new page 68. The 4th line of the abstract
was fncorrectly left out from the original version.
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DISCLAIMER
This report has been reviewed by the Health Effects Research
Laboratory, U.S. Environmental Protection Agency, and approved for
publication. Approval does not signify that the contents necessarily
reflect the views and policies of the U.S. Environmental Protection
Agency, nor does mention of trade names or commercial products
constitute endorsement or recommendation for use.
11
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FOREWORD
The many benefits of our modern, developing, industrial society are
accompanied by certain hazards. Careful assessment of the relative risk
of existing and new man-made environmental hazards is necessary for the
establishment of sound regulatory policy. These regulations serve to
enhance the quality of our environment in order to promote the public
health and welfare and the productive capacity of our Nation's population.
The Health Effects Research Laboratory, Research Triangle Park,
conducts a coordinated environmental health research program in toxicology,
epidemiology, and clinical studies using human volunteer subjects. These
studies address problems in air pollution, non-ionizing radiation,
environmental carcinogenesis and the toxicology of pesticides as well as
other chemical pollutants. The Laboratory develops and revises air quality
criteria documents on pollutants for which national ambient air quality
standards exist or are proposed, provides the data for registration of new
pesticides or proposed suspension of those already in use, conducts research
on hazardous and toxic materials, and is preparing the health basis for
non-ionizing radiation standards. Direct support to the regulatory function
uf the Agency is provided in the form of expert testimony and preparation of
affidavits as well as expert advice to the Administrator to assure the
adequacy of health care and surveillance of persons having suffered imminent
and substantial endangeraent of their health.
This investigation was designed to assess the occupational and
environmental exposure to pesticides in South Florida, an area where
pesticides are widely used. In addition to the conventional approach for
measuring exposure to organophosphates and carbamates by means of
cholinesterase determination, emphasis is given to the study of metabolites
of pesticides in urine, the analysis of pesticide residues in samples of
adipose tissue, and the monitoring of air for pesticide pollution. Attention
is focused on the diagnostic and epidemiologic potential of certain biologic
and environmental indices, such as the urinary metabolite profile and the
concentration of pesticides in air, which are important with regard to the
occupational health and safety of the worker and the protection of the
general population against incidental exposure to pesticides.
John H. Knelson, M.D.
Director,
Health Effects Research Laboratory
iii
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CONTENTS
Page
Title Page .
Disclaimer .
Foreword
Contents
Preface
Abstract .
Figures
Tables
Acknowledgements
Abbreviations and Symbols
I. Introduction . . . .
II. Conclusions .•
III. Recommendations .
IV. Materials and Methods ....
V. Experimental Procedures ....
VI. Results and Discussion ....
References
Bibliography
Appendices
A. General Population Raw Data
B. Adipose Pesticide Residue Raw Data
C. Air Monitoring Raw Data
Glossary
Technical Report Data
i
ii
iii
iv
v
viii
ix
xi
xiii
xiv
1
3
5
6
11
17
56
58
59
66
68
iv
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UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
HEALTH EFFECTS RESEARCH LABORATORY
RESEARCH TRIANGLE PARK
NORTH CAROLINA 27711
June 15, 1977
ERRATA
SUBJECT: EPA-600/1-77-019
April 1977
TITLE: OCCUPATIONAL AND ENVIRONMENTAL PESTICIDE STUDY IN
SOUTH FLORIDA
The following corrections should be made to the above report:
1. Page 17 - first paragraph, lines 7 and 8: 3,5,6-Trichlorophenol
(3,5,6-TCP) should be 3,5,6-trichloropyridinol
C3,5,6-TC Pyridi.nol).
2. Page 18 - Table 4 C: 3,5,6-TCP (after "Chlorpyrifos") should be
3,5,6-TC Pyridinol
3. Page 48 - Table.14: column heading 2,3,5-TCP should be 3,5,6-TC
Pyridinol
4. Page 60 - Appendix A: 3,5,6-TCP [under "phenols") should be
3,5,6-TC Pyridinol
5. Page 68 - Attached is a new page 68. The 4th line of the abstract
was incorrectly left out from the original version.
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PREFACE
OCCUPATIONAL AND ENVIRONMENTAL PESTICIDE EXPOSURE STUDIES IN SOUTH FLORIDA
Possessing a semi-tropical climate and with a year round growing season
Florida is second only to California in pesticide usage. Pesticides are
widely used in agriculture, with citrus, fruits and vegetables being the
chief agricultural products grown. They are also widely used by public
health for vector borne disease control and for the control of nuisance
pests; additionally, various types of different pesticides are used by
homeowners for interior pest control and horticultural purposes. It is
not surprising, therefore, that high priority has been given to human pesti-
cide safety and protection of the environment of Florida.
In the past decade, a community pesticide study in this area amply
demonstrated that there are a wide variety of real and potential human
health hazards which are due to the widespread use of pesticides. The
organophosphates and carbamates are widely used, causing acute systemic
poisonings, and illnesses which are due to topical effect of these pesti-
cides on the skin and in the eye. Ethyl parathion and mevinphos (Phos-
drin) are the two most toxic pesticides used by agriculture. They have
caused numerous incidents of serious pesticide poisonings. Currently
these are seen predominately in the agricultural worker, especially those
workers occupationally exposed to these two more toxic materials.
Today, over 60% of the pesticides used in agriculture in Florida
are applied by aerial application, and systemic poisonings have been identi-
fied in two different types of occupational categories. The first cate-
gory has been the pesticide applicator, and includes people who formulate,
mix, load and apply pesticides, and the second occupational category is
the "picker" group which is composed of a sizeable occupational work force
whose jobs require picking and thinning of crops on a seasonal basis.
Poisonings in these two groups are sometimes called "applicator poisoning"
and "picker poisoning" respectively. Workers in the former category, are
at some time or other exposed to varying degrees of the pesticide concen-
trate. Pesticide mixers and loaders have been found to be the group with
the most exposure and at greatest risk of sustaining systemic poisoning.
The clinical picture is a cholinergic illness exhibiting the symptomato-
logy of parasympathetic stimulation. This is the result of cholinesterase
inhibition in the central nervous system which is confirmed in the labora-
tory by the demonstration of significant inhibition of the red blood cell
and plasma enzymes. Inhibition of these enzymes usually precedes the
appearance of an acute cholinergic illness and this measurement is used
as a surveillance tool of the pesticide applicator since the test has shown
to be a reliable predictor of cholinergic poisoning. Laboratory tests
which are predictive are of major importance to the occupational health
and safety of the worker.
In contrast, picker poisoning, which is also occasionally seen in
this area, involves workers who pick and thin the crops. The exposure
is primarily dermal and is the result of contact with the diluted
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pesticide residues on the leaf of the particular crop. The illness which
results from this is milder than that which is seen in the pesticide
applicator.
Both the applicator and the picker are also prone to dermatitis.
This results either because of the irritant properties of the chemical
or is more commonly due to the allergic makeup of the individual.
These topical lesions are not dose related, and therefore, the magnitude
of the pesticide exposure is not a primary factor, the specific allergic
potential of the individual being the most important variable. This
health effect has not been studied in this project.
Since continued pesticide usage is essential for modern agricultural
technology, occupational health is vitally concerned with the protection
of the exposed workers and with the development of a variety of strategies
which are designed to minimize this exposure. The efficacy of these
interventions are measured in terms of reduction in the amount of pesticide
exposure and through ongoing studies of cholinesterase surveillance of
the workers, especially those workers who are at special risk from working
with the more toxic pesticides. Cholinesterase surveillance, the mainstay
of present pesticide occupational surveillance, has many limitations and
at times is inadequate, non-specific, and unpredictable. Over the last
decade, increased interested has been shown in surveillance by the urinary
metabolites. Human and animal studies have demonstrated that these urinary
metabolites are excellent measures of exposure to the organophosphate and
carbamate pesticides. The potential of these metabolites as a surveillance
instrument has been further stimulated by the significant developments
in analytical methodologies.
Two types of metabolites are identified following exposure to the
organophosphate and carbamate insecticides. These are the alkyl phosphates
and phenolic metabolites, and both are excreted rapidly in the urine
following exposure. With organophosphate exposure, the alkyl phosphate
and phenolic metabolites are the major urinary metabolites, and the phenols
are the major metabolites of carbamates.
Urinary alkyl phosphates (dimethyl phosphates (DMP), diethyl phosphates
(DEP), dimethyl thio phosphates (DMTP) and diethyl thio phosphates (DETP)
appear as metabolites after exposure to the inorganic organophosphorus
pesticides. The urinary dimethyl phosphate and diethyl phosphate are
metabolites of the oxon of the intact pesticides. These metabolites can
result from exposure to the oxidation products of the thio organophosphate
pesticides, to the oxon, or to organophosphates not containing any sulfur
such as DDVP and phosdrin. It is a known fact that oxons are toxic and
inhibit the cholinesterase more than the thio organophosphate pesticides.
To summarize therefore, the major alkyl phosphate metabolites which
can be identified following human exposure to the organophosphates are
the dimethyl thiophosphates (DMTP), diethyl thiophosphates (DETP) and
the dimethyl (DMP) and diethyl (DEP) alkyl phosphates.
vi
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The phenolic metabolites reflect the nitro and chlorophenol moieties
of the insecticides. These two types of urinary metabolites are also
usually excreted rapidly in the urine. Being rapidly excreted they
should prove to be usable indices of recent exposure.
The other major group of pesticides of epidemiological interest
are the organochlorine insecticides. These are stored in fat and
persistent in man as well as in the environment. Their concentrations
in adipose tissue therefore is another biologic index of exposure,
being reflective of long term exposure. The epidemiologic potential
is greatest in studies measuring long term exposures.
Today, man is vulnerable to three types of pesticide exposures;
acute, chronic, and incidental. Acute exposure is an over exposure
in which the illness develops shortly after the over exposure and
is reflective of the known toxicity of the offending pesticide.
Chronic exposure is the exposure of the pesticide worker, that is
usually high and is acquired by working day after day either in the
manufacturing,.formulation, mixing, handling or application of pesticides.
The population at risk is the occupationally exposed. Incidental exposure
is the exposure of the general population; it is ubiquitous and man
receives small amounts of pesticides through trace amounts of resi-
dues found in air, water, food and fiber of his day-to-day living.
The magnitude o£ such exposures can be measured either by determin-
ing the residuea stored in fat and hair or excreted in the urine
of the population at large or can be quantitated by measuring pesti-
cides in the air, water, food and clothing. The latter residues
are environmental indices of pesticide exposures.
The aforementioned strategies have been the basis of our occu-
pational and environmental exposure studies in South Florida. The
urinary metabolites have been the biologic indices used to measure
acute, occupational and incidental exposure of man to organophosphate
and carbamate pesticides. The human pesticide residue profile has
been the biologic index used to appraise occupational and incidental
exposure to the organochlorines in this area. Our environmental
assessment of pesticides has focused on concentrations of pesticides
in air and these have been the environmental index used to appraise
the environmental impact of pesticides in South Florida.
In conclusion, it should be emphasized that all the studies
included in this report have been conducted under natural occurring
events. Exposures have been measured as they have occurred and nothing
artifical has been introduced. Specific dose testing is the more
precise way to correlate biologic responses, conclusions being formu-
lated on the basis of observational data acquired in the field.
vii
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ABSTRACT
In the past, accurate expressions of human pesticide exposures and environ-
mental pesticide contamination have suffered from interpretative difficulties
which have stemmed from the use of biologic indices that were indirect and
nonspecific measures of human exposure (cholinesterase inhibition) and environ-
mental indices which lacked precision due to analytical shortcomings. Our
studies of the urinary pesticide metabolites have demonstrated that the
alkyl phosphates are highly sensitive expressions of recent human exposures
to the organophosphate group of pesticides. Urine phenolic metabolites are
both sensitive and specific indicators of recent individual organophosphate
and carbamate exposures. In addition, the modification of the analytical
procedures for pesticides in air and in fat have greatly enhanced the breadth
and reliability of estimates of pesticides in the air and have facilitated
the recognition of the less polar organophosphate insecticides in human fat.
Because of the sensitivity of our modified methodology, the urinary
alkyl phosphates were found to be ideal diagnostic tools of acute pesticide
poisonings and epidemiologic measures of subtle and minute differences in
organophosphate exposures, a property which lends itself to human monitor-
ing of incidental organophosphate exposure and to epidemiologic studies
of the occupationally exposed worker. Because of a lack of specificity
for individual organophosphate exposures, however, the alkyl phosphates
did not appear to be satisfactory surveillance instruments of the occupa-
tionally exposed workers when cholinesterase inhibition or illness was
the disease end point of primary concern, and when exposures were to a
mixture of pesticides whose toxicities varied considerably. Only in occu-
pational exposures to a single pesticide, particularly to those that have
a high toxicity, can these urinary metabolites be used as a surveillance
instrument. The usefulness of the alkyl phosphate studies to recognize
minute organophosphate exposures permitted the recognition of important
and unrealized sources of worker exposure which stemmed from concentrations
of pesticides in the air of the work environment and in worker's clothing.
The recognition of bromophos, a fat soluble organophosphate, in the
fat of three of the five formulators emphasized the continuing need for
human monitoring with newer methodologies to encompass the less polar organo-
phosphates as well as the organochlorine pesticides.
With improvements in air monitoring procedures, the major source of
pesticide contamination in air was found to be in areas where pesticides
are indiscrimately mixed and loaded in the field and inside the formulating
plant. In other areas of South Florida, aerial contamination of pesticides
was minimal.
viii
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FIGURES
Number Page
1 Selected air sampling sites in South Florida 10
2 Sequential urinary excretion of diethyl alkyl phosphates in
four farm workers hospitalized due to 10% ethyl parathion
granular dermal exposure 19
3 Sequential urinary excretions of diethyl alkyl phosphates in
three cases of poisoning by 6% ethyl parathion mixtures due
to spillage of the concentrate 20
4 Sequential excretion of dialkyl phosphates and phenolic
metabolites following accidental oral ingestion of dursban
in a 3 year old black male 21
5 Sequential excretion of dialkyl phosphates and phenolic
metabolites following accidental oral ingestion of dursban
in a 3 year old black female 22
6 Serum concentrations of dichlofenthion (ppb) and red cell
and plasma cholinesterase levels (^pH/hr) during recovery
following oral ingestion of dichlofenthion (VC-13) • 24
7 Urinary excretion of alkyl phosphates and phenolic metabolites
of dichlofenthion (VC-13) poisoning. Dade County 1974 .... 25
8 Sequential BMP excretion (ug/hr) in a case of occupational
phosdrin poisoning (dermal) in a 39 year old black male
(B.M.) 26
9 Sequential excretion of malathion mono-acid (MMA) malathion
di-acid (MDA) urinary metabolites following oral ingestion
of an unknown amount of malathion concentrate 27
10 Sequential excretion of urinary alkyl phosphates in a mixer
loader (T.J.) whose red blood cell cholinesterase was 0.60
ApH/hr and plasma cholinesterase 0.55 APH/hr during a
pesticide exposure to dimethoate (Cygon) and dibrom 32
ix
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FIGURES - Continued
Number Page
11 Sequential excretion of urinary alkyl phosphates and para-
nitrophenol in a mixer-loader (J.L.) whose red blood cell
cholinesterase was 0.11 ApH/hr and plasma cholinesterase
0.10 ApH/hr during a mixed exposure to pesticides .... 33
12a Comparison of mean urinary alkyl phosphates in workers
wearing fluorocarbon treated and untreated clothing . . 41
12b Comparison of mean urinary alkyl phosphates in workers
wearing fluorocarbon treated and untreated clothing . . 42
13a Frequency distribution of organochlorine residues in
adipose tissue of the Dade County general population . . 51
13b Frequency distribution of organochlorine residues in
adipose tissue of the Dade County general population . . 52
x
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TABLES
Number Page
1 Essential steps of the F.D.A. procedure showing the pesti-
cides identified in three fractions 14
2 Additional pesticides identified in four fractions by the
modified method described 15
3 Detectability limits (ng/m ) for ethylene glycol impinger
using silica gel column 16
4 Pesticides and their major metabolites identified in some
of the poisoning cases and described in this report . 18
5 Pesticide exposure history of two aircraft mixer-loaders,
before and during the period of urinary alkyl phosphate
surveillance. South Florida, 1975 29
6 Urinary alkyl phosphate metabolite studies in a mixer-loader
(A) having a normal cholinesterase level and whose pesti-
cide exposure was to dimethoate (Cygon) and dibrom.
Belle Glade, Florida, 1975 30
7 Urinary metabolite studies in a mixers-loader (B) having an
inhibited cholinesterase and whose work exposure was to
a variety of pesticides. Belle Glades, Florida, 1975 . 31
8 Comparisons of mean and ranges, and ratios of urinary alkyl
phosphate metabolites (ug/ml) in two mixer-loaders found
to have normal (A) and inhibited (B) cholinesterase
levels 35
9 Unadjusted and adjusted (for osmolar corrected) mean differ-
ences in urinary alkyl phosphate levels between agricul-
tural workers wearing untreated and treated clothing . 38
lOa Comparison of the adjusted osmolar mean of twelve hour
urinary alkyl phosphates (ug/ml) in workers wearing un-
treated clothing and workers wearing fluorocarbon
treated clothing over a six day period 39
XI
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TABLES - Continued
Number Page
lOb Comparison of the adjusted osmolar mean of twelve hour
urinary alkyl phosphates (ug/ml) in workers wearing
untreated clothing and workers wearing fluorocarbon
treated clothing over a six day period 40
11 Mean and ranges and frequency of identification of alkyl
phosphates and selected phenols in the general population
of Dade County, Florida, 1975 43
12 Cholinesterase and urinary alkyl phosphate findings before,
during, and after orange juice ingestion 44
13 Simultaneous adipose and serum concentrations of pesticides
in five formulators, 1975 46
14 Simultaneous cholinesterase and urinary alkyl phosphate and
phenolic metabolites of pesticides in five formulators,
Dade County, Florida, 1975 48
15 Comparison of adipose organochlorine pesticide residues (ppm)
in Dade County population (adults), 1975 and 1970 50
16 Medians and ranges of air concentrations (ng/m^) of pesticides
observed in locations with repeated air sampling surveys,
South Florida, 1975-76 53
17 Air concentrations (ng/nH) of pesticides and their ranges at
four occupational work sites in South Florida, 1975 54
xii
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ACKNOWLEDGEMENTS
The investigators acknowledge with gratitude the cooperation and assistance
offered us to conduct these studies by Ag-Air Flying Service, Allied Heli-
copter Service Inc., Tri-State Dusting Service, U.S. Department of Agri-
culture, Dade County Parks Department, Woodbury Chemical Company, and
Jackson Memorial, Hialeah, Glades General and Baptist Hospitals as well
as the several volunteers representative of the general population for
their willing cooperation and participation to provide blood, urine
and adipose samples for appropriate cholinesterase, urinary metabolites
and adipose residue studies.
In addition, the investigators at the University of Miami appreciate the
advice and guidance provided by Drs. Thomas Scotti and William Durham,
and Mr. Jack Thompson and Mr. Frank Wilinski from Research Triangle Park,
North Carolina, and Dr. T. M. Shafik and Miss Anita Peoples, both members
of our Department.
xiii
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List of Abbreviations and Symbols
a BHC
8 BHC
Y BHC
ChE
DDVP
A pH/hr
DEP
DETP
DMDTP
DMP
DMTP
EC
Et. parathion
evap
FDA
FPD
GLC
HC1
HCB
Hep. Epox.
3
m
MDA
MeCl
Me. parathion
mg/kg
ml
alpha benzene hexachloride
beta benzene hexachloride
gamma benzene hexachloride
cholinesterase
dichlorvos
delta pH per hour
diethyl phosphate
diethyl thiophosphate
dimethyl dithiophosphate
dimethyl phosphate
dimethyl thiophosphate
electron capture detectors
Ethyl parathion
evaporate
Food and Drug Administration
flame photometric detector
gas liquid chromatography
hydrochloric acid
hexachlorobenzene
heptachlor epoxide
cubic meter
malathion di-acid
methylene chloride
methyl parathion
milligram per kilogram
milliliter
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ml/Osm/1
MMA
Na2S04
NH4C1
ND
, 3
ng/m
PGP
PNP
ppb
ppm
/
yg/ml
vs.
milliliter per milliosmols per liter
malathion mono-acid
sodium sulfate
ammonium chloride
not detected
nanogram per cubic meter
pentaehlorophenol
paranitrophenol
parts per billion
parts per million
microgram per milliliter
vs.
xv
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SECTION I
INTRODUCTION
Descriptive epidemiologic studies of South Florida have shown that
there are many serious health problems with present pesticide management
practices (1,2). Use pattern surveys in the same area have shown that
large amounts of pesticides are used (3,4) but what is not known is
the true magnitude of the consequences of such exposures in terms of
human and environmental effects. The data which have already been collected
are generally descriptive and anecdotal and more precise information is
needed.
Reliable biological and environmental expressions of this contamina-
tion will provide the information which is urgently sought. Insofar as
humans are concerned, biologic indices are the preferred instruments for
epidemiological appraisal of the situation. For environmental studies, air
sampling has reached a high degree of sophistication and is the preferred
environmental index of exposure. If these separate indices are both sensi-
tive and specific, health and environmental effects of pesticides can be
reliably quantitated.
In the first two years of this project, our studies of acute poison-
ing cases and occupational exposure studies had suggested that urinary
alkyl phosphate and phenolic metabolites were sensitive indicators of
worker exposure to certain organophosphates and carbamates (5,6). Signi-
ficant inverse correlations of cholinesterase levels with alkyl phosphate
urinary metabolites were demonstrated under worker exposure to 6-3 ethyl
methyl parathion mixtures and mevinphos. DMTP and DETP, and DMP and DEP
were the four alkyl phosphate metabolites identified in these exposures.
Both quantitative and qualitative information was provided from the alkyl
phosphate data. Concentrations of DEP of >0.4 ug/ml were observed in
all of the first urines of seven poisonings with ethyl-methyl parathion
and these urinary concentrations were in striking contrast to the levels
of DEP observed in asymptomatic occupationally exposed workers, where
of 99 urines only 1 had concentrations greater than 0.4 ug/ml. The
DEP/DETP ratio was also very highly informative because the mean of
this ratio for these two metabolites was 4.14 in poisoning cases com-
pared to 0.88 in occupationally exposed workers. This, therefore, was
evidence of one biologic index that promised to be a reliable indicator
of acute and occupational exposure of the agricultural worker. Being
rapidly excreted from the body, the metabolites provide retrospective
information on recent exposures especially acute poisoning. Being
also sensitive measures of minimal pesticide exposure it was planned
to test their reliability in intervention studies designed to limit
worker exposure and also to measure the incidental exposure of the
general population in the area.
Earlier studies had also demonstrated that a fat soluble organophos-
phate compound could be detected in human fat in a poisoning case (7),
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Finally, earlier monitoring studies had also demonstrated signi-
ficant differences in air concentrations of pesticides, suggesting
that pesticides in air would be a most useful way of expressing environ-
mental air pollution and appeared to be the best environmental index
to quantitate the environmental effects of pesticides in this area.
The studies described hereinafter have been designed to expand
these earlier findings with the intent of testing the urinary pesticide
metabolites as diagnostic and surveillance instruments and exploring
their potential as epidemiologic instruments in organophosphate and
carbamate exposures. Additionally, adipose residue studies have been
conducted to determine occupational and general population exposures
and to find out whether any organophosphates were now being stored
in fat; air sampling of pesticides has been continued in order to
determine environmental exposure to pesticides in this area.
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SECTION II
CONCLUSIONS
This year these occupational and environmental pesticide studies in
South Florida have sought to measure pesticide exposure by testing the
urinary pesticide metabolites as indices of recent exposure and the adi-
pose residue as indices of the more chronically sustained exposures parti-
cularly those acquired from organochlorine pesticides. The environmental
assessment of pesticides has been based mainly on air sampling of pesti-
cides in different sample sites selected on the basis of being reflective
of low, average and high pesticide usage.
The urinary metabolites have been used to measure human exposures in
acute poisonings.in the occupationally exposed,and in the general popula-
tion, in order to test (1) the diagnostic potential of the pesticide meta-
bolites in acute poisoning, (2) the surveillance potential of the metabolites
where surveillance has been equated with the assessment of the predictive
potential for cholinesterase depression or illness, and (3) the epidemic-
logic evaluatory potential of the metabolites in exposures to the organo-
phosphate group rather than to a single pesticide.
The diagnostic potential in acute poisoning was amply demonstrated
by a series of case studies wherein sequential urines were analyzed during
the early phase of the poisoning. If the organophosphate exposure which
caused the illness was due to a single pesticide, especially if the pesti-
cide was metabolized to alkyl phosphate and phenolic metabolites, then
highly specific diagnostic laboratory data were obtained. If, however,
the poisoning was the result of a mixture of organophosphates then the
identification of the causal pesticides was impossible since the urinary
alkyl phosphate metabolites are group specific (dimethyl or diethyl)
rather than pesticide specific.
The initial concentrations of the urinary pesticide metabolites in
poisoning were related to (1) the chemical configuration of the pesticide,
(2) its metabolism and toxicity (LDso) and (3) the dose and route of
absorption. Of these several variables influencing initial urinary concen-
trations of metabolites, it was found that the dose and toxicity were the
most important. The dialkyl phosphates, reflective of the oxon appeared
to be more specifically related to cholinergic illness, than did the di-
thio urinary derivatives. For example, in 32 of 40 urines analyzed from
seven poisonings cases due to ethyl parathion, DEP concentrations were
higher than DETP.
In the study of these metabolites in the occupationally exposed, the
same problems with mixed exposures were encountered. Almost all workers
were exposed to a variety of pesticides whose toxicities varied consider-
ably.
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The urinary alkyl phosphates while being highly sensitive indicators
of organophosphate exposures, lacked specificity for individual organo-
phosphate pesticides, making it impossible to uniformly predict cholines-
terase inhibition illness on the basis of a single urinary alkyl phosphate
concentration. Thus, with unknown organophosphates, surveillance was
impossible. The only exception to this was with workers working with
ethyl parathion or mevinphos where cholinesterase depression might be
anticipated. Based on findings of these studies, the urinary metabolites
could be used as survellance instruments and DEP concentrations greater
than 0.9 ug/ml with parathion, or DMP concentrations greater than 1.0 ug/
ml in cases of mevinphos exposure, would be regarded as dangerous levels
justifying temporary withdrawal of the worker from exposure to these
particularly toxic members of the group.
In contrast to specificity, however, sensitivity of these indices
was remarkable, often facilitating the identificiation of minute exposures
from the environment or from contaminated clothing which was not recognized
by the worker himself. It was concluded that the urinary alkyl phos-
phates were very reliable epidemiologic instruments of organophosphate
exposures capable of identifying subtle differences in groups of workers
and able to measure small incidental exposure of the general population
to these pesticides in the environment.
The adipose pesticide residues showed that (1) fat soluble organophos-
phate storage was occurring in the formulators, and (2) that there is
significant worker exposure from pesticide concentrations to clothing (8)
and pesticides in the air of worker's environment. Many of the organo-
chlorine pesticides identified in adipose residues had not been recently
formulated but the identification of these in the air of the work environ-
ment was the major factor contributing to the continued exposure of these
obsolescent pesticides.
In the air sampling studies it was concluded that pesticides were
minimal in the suburban and urban areas but higher concentrations were
found in the work environment.
-------
SECTION III
RECOMMENDATIONS
Based upon our studies, the following additional steps are recommended:
1. Verification of alleged pesticide poisoning incidence by
confirmatory urinary metabolite data.
2. Testing selected applicator surveillance programs by
urinary metabolite surveillance when highly toxic pesti-
cides are being formulated or applied.
3. Urgent research on the role of contamination of worker's
clothing is needed, making use of the urinary metabolite
data to measure this contamination, and residues in the
clothing itself, and investigating the potential of treat-
ing clothing with fluorocarbon as well as laundering
efficacy.
4. Fat soluble organophosphate insecticide studies - it is
recommended that environmental human health effects of
these less polar insecticides be .further investigated.
5. Monitoring programs - The prevalence of incidental expo-
sure of the population at large to organophosphates and
carbamates needs expanded research and the sources of
these pesticides and their metabolites in food warrant
further study.
6. Urinary alkyl phosphate data should always form part of
the epidemiologic studies which measure organophosphate
exposures. Thus, re-entry studies, new formulation
studies, etc. should all be evaluated on the basis of
urinary metabolite data.
7. Air monitoring of pesticides should be continued in South
Florida especially now that open-air burning of containers
is being planned.
-------
SECTION IV
MATERIALS AND METHODS
1. Urinary Pesticide Metabolite Studies
a. Acute poisoning cases - Arrangements were made with physicians and
nurses in the Emergency Rooms and Intensive Care Units of Jackson Memorial
Hospital, James Archer Smith Hospital, Hialeah Hospital and Belle Glades
General Hospital to call us as soon as a pesticide poisoning case was admitted
to the hospital. A program was instituted whereby all urines voided during
the first two or three days were collected in hexane washed jars, labelled,
and frozen at 5 C for later urinary metabolite determinations. 10 cc of
blood were collected in a heparinized tube and 10 cc of clotted blood were
also collected; the former for red blood cell and plasma cholinesterase
determinations and the latter for intact pesticides. Subsequent hospital
and field visits were made by project personnel to review and document
the clinical findings and to determine the mechanism of the poisoning and
the most probable route of absorption. Sequential urines were obtained
from eleven cases of systemic poisonings due to organophosphate pesticides.
Seven of these poisonings were due to ethyl parathion and all were the
result of dermal exposures; four were the result of occupational exposure
to 10% ethyl parathion granular formulation and three were the result of
occupational exposure to 6% ethyl parathion mixutres. Three cases of mevin-
phos (Phosdrin) poisoning were similarly investigated but only one is pre-
sented in this report, and two cases of chlorpyrifos (Dursban) poisoning
due to ingestion of the insecticide and one case of malathion poisoning
also due to ingestion are included. All patients were hospitalized
shortly after becoming sick so that the initial urine voided almost
certainly represented the first voided specimen after developing overt
illness.
b. Occupational studies; (a) Pesticide application and loading ex-
posure studies - Two mixer loaders (A and B), one with normal cholinester-
ase levels (A) and one with significant cholinesterase depression (B),
agreed to provide all voided urine specimens over a continuous work period
of between 4 and 5 days. These specimens were collected in hexane washed
jars, and the date and time of voiding noted. The volume of the urine
voided was measured and the specimen frozen to be analyzed at a later date
for alkyl phosphate and phenolic metabolites. Prior to analysis, urine
osmolality determinations were made using the Fiske osmometer (9) and
urinary alkyl phosphates were corrected to a standard osmolality of 800
ml/Osm/1.
(b) Pesticide pickers and foliar residue exposure studies - "Picker
poisoning" is not a serious problem in South Florida and in order to ex-
plore the potential of protective clothing in the field in the prevention
of foliar residue exposure, the Department of Epidemiology and Public
Health conducted a field study in El Salvador. This research was an
independent project not supported by the U.S. Environmental Protection
Agency, however, these activities afforded an opportunity to investigate
the sensitivity of the urinary alkyl phosphate metabolites as an epidemic-
-------
logic Instrument in these studies. These urinary metabolite data, therefore,
were included in these studies in order to throw some light on the overall
goals of the E.P.A. supported studies concerned with occupational and
environmental pesticide exposure studies.
Twenty seven agricultural laborers picking cotton in El Salvador were
asked to participate in a protective clothing project where each would
be provided with new sets of long-sleeved shirts, denim pants, cotton
socks and heavy leather shoes purchased in a local market. Fourteen workers
were given clothing which had been pretreated by spraying with a fluoro-
carbon solution provided by the 3M Company. Earlier laboratory studies had
shown that penetration was reduced when a cloth was treated with a fluoro-
carbon solution and then sprayed with a 10% xylene dye extract. Thirteen
workers were given new but untreated clothing.
The Ministries of Health and Agriculture had requested this field study
and participated in the field testing of the protective clothing. The
nature of the study was explained to each of the volunteers and signed
consent forms obtained.
During the six day study period, urines were collected consecutively
at 12 hour intervals in hexane washed bottles. Aliquots were frozen and
later analyzed by the Miami Pesticides Laboratory. Osmolality was measured
by the Fiske osmometer (9). Urines with osmolar concentrations under 100
ml/Osm/1 were excluded under the assumption that they were not valid speci-
mens. All values of alkyl phosphates at or below the limit of detectability
were treated as zero in all calculations.
The fields were hot and dry, and temperatures during the six days
ranged from 63° F at night to 80° F during the day. The fields had been
sprayed from the air with mixtures of ethyl and methyl parathion five
days before the study began. Chlordane, toxaphene and methomyl were also
in use.
c. General Population Studies: (a) Urinary alkyl phosphates and
phenolic metabolite studies - Grab samples of urine were collected in hex-
ane washed jars, each specimen was labelled with the name, age, race, sex
and occupation of the participant. These were analyzed for alkyl phos-
phate and phenolic metabolite data and the concentration of the metabolite
corrected to a uniform osmolality of 800 ml/Osm/1.
(b) Orange juice feeding study - In order to determine whether
orange juice ingestion was a source of incidental general population ex-
posure to the organophosphates, two volunteers agreed to ingest one quart
of orange juice for three days and to provide all urines voided between
9:00 a.m. and 4:00 p.m. Pre-exposure urines were collected over the same
time period for two days before ingestion and for two days after ingestion.
Pre and post cholinesterase determinations were made in both volunteers..
The orange juice was analyzed for alkyl phosphates.
The analytical procedures used for these several studies for the
alkyl phosphates was the Shafik et al method (10) which has been modified
and is described under "Experimental Procedures" and for the phenolic meta-
bolites the Shafik et al method (11). For the malathion mono and di-acid
-------
metabolites the Shafik and Bradway method (12) was used. The Michel method
(13) was used for the cholinesterase determinations.
2. Adipose Pesticide Residue Studies
a. Occupational exposure studies (formulators) - Adipose body burdens
of pesticides together with environmental and biological surveys were
studied in a group of five formulators working in a formulating plant.
After explaining the nature and purpose of this study to the workers
a signed consent form was obtained from each, agreeing to participate in
this study and agreeing to provide a single blood, fat and urine sample
in order to measure the total body burden of pesticides being sustained
in this type of occupation.
The five formulators who wore respirators, rubber gloves, boots,
rubber aprons and coveralls which were changed daily, mixed and formulated
a wide variety of pesticides from 8:00 a.m. to 12 noon and then from 1:00
p.m. to 5:00 p.m.; they worked 5% days per week.
J.P., the plant supervisor has worked in the formulating plant for
15 years and A.P., the senior and most experienced formulator has worked
in the plant for 18 years. T.W. and J.T. have been employed for three
years and E.W. (T.W.'s brother) has worked only four months.
The plant where the men work is a 40 x 200 ft. concrete block build-
ing with a high pitched steel corrugated roof. The walls are 8 ft. high
and there are 6 - 12 ft. doors; 3 on each wall to provide cross ventila-
tion. Additional ventilation is supplied by 2 - 4 ft. exhaust fans near
the peak of the ceiling structure. The offices are located in the north
end of the building; and approximately three quarters of the area is occu-
pied by columns of 55 gallon pesticide drums, cardboard and paper packages
containing granular and powdered mixtures of different types of pesticides.
The only formulation done takes place at the south end of the building.
Here, there are two closed-system formulation vats for liquid pesticides
with listed capacities of 500 and 165 gallons each. In addition, there
is a semi-automatic roller mixer for granular and powdered formulations
which mixes 50 cubic feet.
Storage of the formulated products consisting of drums and bags are
as described above with center lane thorough fares with side aisles; all
materials are placed on pallets.
Between 1 and 2 gms of fat were obtained from the gluteal region
from each of the volunteers under aseptic conditions and under local anes-
thetic by a board certified surgeon at the University of Miami Hospitals
and Clinics. The specimens were placed in hexane washed jars with alum-
inum foil screw top caps, frozen and later analyzed by gas chromatography
using electron capture and flame photometric detectors for organophosphate
pesticides.
b. General population adipose studies - 20 surgical biopsy specimens
from a random group of patients coming to surgery at Jackson Memorial Hospi-
tal Dade County, Florida were obtained. Between 1 and 2 grams of fat were
collected from the surgical site, placed in hexane washed jars, frozen
and later analyzed.
-------
The Sherma and Shafik (14) method was modified for organochlorine
and organophosphate determinations and is listed under "Experimental Pro-
cedures." The urines were analyzed by the Shafik et al. (10) method and
cholinesterase determinations were analyzed by the Michel (13) method.
3. Air Monitoring Studies
Forty air monitoring samples for pesticides were analyzed and some
of the selected sites are shown in Figure 1. Twenty four hour samples
were collected using an M.R.I, air sampler equipped with four impingers
charged with 400 ml of. ethylene glycol. Each set of impingers was used
for 12 hours to collect the 24 hour air sample. The standard F.D.A. (15)
procedure has been modified by extracting the ethylene glycol with methy-
lene chloride and chromatographed on a silica gel column. A modification
of the Sherma and Shafik method (14) for analysis of pesticides in air
was used and modified as described in "Experimental Procedures."
-------
BIMINI
MIAMI
1. Suburban
2. Everglades
3. Bimini
4. Airport
5. Formulating Plant
6. Aerial Applicator
7. Aerial Applicator (H)
8. Storage Shed
Figure I. Selected air sampling sites in south Florida
LQ
-------
SECTION V
EXPERIMENTAL PROCEDURES
1. Urinary Alkyl Phosphate Methods Development
The measurement of alkyl phosphates in urine using an amberlite resin
was modified to enable the analysis to be performed rapidly, efficiently
and accurately.
Urine is diluted with acetone and collected on an Amerlite CG400
resin. This resin is placed in a culture tube containing .05 ml 6 NHC1
and 1 ml acetone. After 30 minutes 3 ml of diazopentane is added and the
derivatization is complete in one hour. The diazopentane derivaties are
extracted with hexane and are concentrated to 1 ml for injection into
the gas chromatograph equipped with an FPD detector. An OV-210 column
that has been treated with carbowax allows for definition of all alkyl
phosphates in one sample.
Urine was spiked with 0.5 ppm, 0.1 ppm and 0.05 ppm alkyl phosphates,
diluted with acetone, concentrated on the Amberlite resin and derivatized
with diazopentane.
Recovery of alkyl phosphates from urine:
DMTP DETP DMP DEP
0.05 ppm 64% 82% 80% 90%
0.1 ppm 63% 84% 80% 91%
0.5 ppm 68% 78% 86% 80%
This technique proved useful and practical as 30 urine samples could
easily be analyzed per day.
Urinary inorganic phosphates are also derivatized by diazopentane
and while they do not interfere with alkyl phosphate peaks they do slow
down the analysis by showing up as very large and very late peaks.
At least 10 ml of urine were made alkaline with KOH in order to preci-
pitate inorganic phosphates in the urine. After centrifugation, this urine
was made acid with HC1 and a complex was formed with the remaining phos-
phate ions by the addition of ammonium molybdate. This complex was pre-
cipitated by safranin and the resultant supernatent was distilled with
acetone and poured through resin as usual. These procedures resulted in
a large decrease of inorganic phosphates but the results varied with differ-
ent urines probably because of the amount of phosphate present in the urine
due to dietary habits.
11
-------
A problem arose concerning the reagent, diazopentane or more speci-
fically the nitroso guanidine. A reagent blank had also shown a few in-
terfering peaks but posed interpretive problems with concentrations just
above the limits of detectability.
After much correspondence and communication with the guanidine source,
we decided to use another derivative, and are presently using 3-benzyl-l-
0-tolytriazine. Preliminary results are very promising. There is a possi-
bility of having a "one tube" analysis and no interference with inorganic
phosphates.
2. Adipose Pesticide Residue Studies - Partitioning for chlorinated and
organophosphate pesticide inadipose tissue
The Sherma and Shafik method (14) for pesticides in air was modified
for combined chlorinated and organophosphate pesticide residue studies
in adipose tissues. Two hundred milligrams of fat were weighed and extrac-
ted three times with 2.5 ml of acetonitrile in a #22 Duall homogenizer.
Each extract was transferred to a 45 ml centrifuge tube. The acetonitrile
extract was evaporated to a volume of 4 ml to which 25 ml of 2% NA2S04
solution was added and mixed in a Vortex mixer. This was extracted with
one 5 ml and two 2 ml portions of methylene chloride, transfering each
extract to the same 13 ml centrifuge tube. The extract was concentrated
to dryness with a keeper solution (1% paraffin oil in hexane) and 0.5 ml
of hexane was added and then subjected to silica gel column chromatography
cleanup.
In the Sherma and Shafik method, the column was washed with 10 ml of
hexane and 0.5 ml of the sample was transferred to the column to obtain
the first fraction. The second fraction was separated by adding 15 ml
of 60% benzene in hexane, and the third fraction was obtained by adding
15 ml of 5% acetonitrile to benzene. The four fraction was extracted
with a 15 ml solution of 50% methylene chloride and benzene.
The lower limits of detectability of this modified method were: p»p'-
DDT 0.05; p,p'-DDE 0.02; o,p'-DDT 0.04; oxychlordane 0.02; HCB 0.01; BHC
0.02; heptachlor epoxide 0.01; dieldrin 0.019; ronnel 0.06; methyl para-
thion 0.09; ethyl parathion 0.12; trithion 0.23; ethion 0.12; chlor-
fenthion 0.05; chlorpyrifos 0.06; diazinon 0.06; and malathion 0.19 ug/ml.
3. Air Monitoring; Studies - Modification of the Sherma and Shafik method
The standard F.D.A. procedure (15) for extracting and analyzing pesti-
cides in air involves extraction of ethylene glycol with hexane, fluorosil
column chromatography and collection of three fractions. Each fraction
contains the pesticides shown in Table 1. The number of pesticides that
could be analyzed by the F.D.A. or M.O.G. procedure were limited by the
solubility of hexane and those pesticides which could be eluted from the
fluorosil column. Table 2 illustrates the new modifications developed by
12
-------
Thompson and Reed at Research Triangle Park, N.C., and Shafik, Barquet
and Morgade at the University of Miami Pesticides Research Laboratory.
Here, the ethylene glycol is extracted with methylene glycol, chromato-
graphed on a silica gel column which permits the collection of four frac-
tions. As shown in Table 2, the number of pesticides which can be ana-
lyzed greatly increased when this modified was used. The lower limits
of detectability of these pesticides are shown in Table 3. The limits
ranged from 0.1 - 2 ng/nr* for chlorinated pesticides; 0.2 - 2.5 ng/m3
for organophosphate compounds and 3-16 ng/m^ for carbamates.
13
-------
Table 1. Essential steps of F.D.A. procedure showing the pesticides identified in three fractions
100 ml ethylene glycpl = 20 m air/6 hrs
350 ml 2% Na.SO.
L. H
3 x 60 ml hexane
Combined hexane extracts
Wash 2 x with 50 ml
Pass through 2 inch x 22 mm id Na SO. column
Evaporate to 3 ml
22 gm florisil column chromatography
4 inch x 22 mm id
Fraction I
Fraction II
Fraction III
200 ml 5% E-PE
5.0 ml/ul; OV-17/QF-1 and
SE-30/QF-1; EC
a-BHC p,p'-DDE
3-BHC o,p'-DDE
y-BHC Perthane
Lindane p,p'-DDD
Heptachlor o,p'-DDT
Ronnel p,p'-DDT
Aldrin Ethion
Hep. Epox. Chlordane
o,p'-DDE
Chlorobenside
200 ml 15% E-PE
5.0 ml/5 ul; OV-17/QF-1 and
SE-30/QF-1; EC
Dieldrin
Endrin
Thiodan
Thedion
2,4-D esters
2,4,5-T esters
1.0 ml/5 ul; SE-30/QF-1; FPD
Diazinon
Ethyl parathion
Methyl parathion
200 ml 50% E-PE
1.0 ml/ 5 ul; SE-30/
QF-1; FPD
Malathion
-------
Table 2. Additional pesticides identified in four fractions by the modified method described
100 ml ethylene glycol = 20 m air/& hrs
600 ml 2% Na SO,
40 ml
MeCl extract
Wash 3 times
Evap. to dryness
.Silica gel chromatography: 1 g. 20% H,.
Fraction I
10 ml Hexane
a BHC HCB
Aldrin Heptachlor
p,p'-DDE Chlorbenside
o,p'-DDT a Chlordane
p,p'-DDD y Chlordane
p,p'-DDT Toxaphene
Fraction II
15 ml 60% benzene in hexane
Fraction III
15 ml 5% CH2CN in benzene
Y BHC
3 BHC
Hep. Epox.
Dieldrin
Endrin
Methoxychlor
Endosulfan I
Endosulfan II
Ronnel
Me. Parathion
Trithion
Et. parathion
Ethion
Dursban
Dichlofenthion
Fenthion
Phorate
Bromophos
Dioxathion
Diazinon
Malathion
Phosdrin
DEF
Baygon
Landrin
Carbofuran
Matacil
Zectran
Carbaryl
Mesurol
Dichlorvos
Fraction IV
15 ml 50% MeCl3 in acetone
Diazinon
Dimethoate
Phosphamidon
-------
Table 3. Detectability limits (ng/m ) for ethylene,
glycol impinger using silica gel column
a BHC
Aldrin
p,p'-DDE
o,p'-DDT
p , p ' -DDD
p,p'-DDT
Y BHC
A BHC
Hep . Epox .
Dieldrin
End r in
a Chlordane
Y Chlordane
B BHC
0.1
0.2
0.3
0.6
0.8
0.9
0.1
0.2
0.3
0.3
0.7
0.2
0.3
l.Q
Heptachlor
HCB
Chlorbenzide
Methoxychlor
Endosulfan
Thiodan II
Ronnel
Me. Parathion
Et. Parathion
Trithion
Ethion
Diazinon
Malathion
0.1
0.1
0.7
3.0
0.2
0.2
0.3
0.6
0.8
2.0
1.0
0.2
1.0
Chlorpyrifos
Dichlofention
Phorate
Me. Bromophos
Mevinphos
DBF
Fenthion
Dioxathion
Carbofuran
Carbaryl
Mesurol
Propoxur
Land r in
0.3
0.2
0.1
0.7
0.5
1.4
0.9
2.5
10.0
16.0
4.0
3.0
4.0
(a)
Based on GLC peaks giving 10% full scale deflection (electron capture),
or a signal to noise ratio 4:1 (flame photometric) above the background
of reagent blanks.
Toxaphene was identified but could not be quantitated because it had 12
peaks in the chromatograin
16
-------
SECTION VI
RESULTS AND DISCUSSION
A. Results
1. Acute Pesticide Posioning Studies
The objective here is to determine the diagnostic potential of the
urinary alkyl phosphates. The major types of urinary metabolites detected
in the urine of poisoning cases will vary with the chemical composition
of the pesticide. Thus, with ethyl parathion, the diethyl phosphate (DEP)
and the diethyl thiophosphate (DETP) and paranitrophenol (PNP) are the
major alkyl phosphate and phenolic metabolites identified„ With chlorpyri-
fos (Dursban) the diethyl alkyl phosphates, DEP, DETP and the phenol 3,5,
6-trichlorophenol (3,5,6-TCP) are the major metabolites excreted; and with
mevinphos (Phosdrin) the dimethyl phosphate (DMP) is the major metabolite
observed. In the case of malathion, DMP, DMTP and DMDTP, the alkyl phos-
phate metabolites of this pesticide are the minor metabolites, and mala-
thion mono-acid and di-acid metabolites are the major metabolites recognized.
The thio derivatives are usually reflective of the parent compound and
the dialkyl phosphates are reflective of the oxon. Table 4 lists the pesti-
cides and the major metabolites identified in some of the poisoning cases
and in occupational workers described in this report.
(a). Poisoning by diethyl organophosphate insecticides - Figure 2
shows the excretion pattern of DEP and DETP in four patients poisoned by
dermal exposures-to 10% ethyl parathion granular formulations and Figure
3 illustrates the excretions of some of the metabolites in three patients
exposed to 6% ethyl parathion mixtures. Metabolite concentrations were
greater in the 10% exposure than in the 6% exposures, the initial concen-
tritions of DEP ranged from 8.1 to 0.9 in these seven poisoning cases.
Initial DEP concentrations were greater than DETP in five of the seven
cases, and in 32 out of 40 urines analyzed in this series suggesting the
significant contribution of the oxon to these intoxications. Figures 4
and 5 illustrate the excretion of DEP, DETP and 3,5,6-TCP in two children
who were poisoned as a result of ingestion of an unknown amount of chlor-
pyrifos. It will be noted that the initial urinary concentrations of DEP
were 30 - 20 ug/ml respectively and were of a much greater order of magni-
tude than seen in cholinergic illness due to ethyl parathion; emphasizing
the importance of the dose and the LD50 of the organophosphate from which
the alkyl phosphate was metabolized rather than the absolute level of the
DEP itself. Here too, in these cases, for the most part, DEP concentra-
tions exceeded the DETP concentrations.
The significance of the physical-chemical properties of the pesticide
causing the poisoning on the duration of metabolite excretion is exempli-
fied by a dichlofenthion (VC-13) poisoning case reported in our annual
17
-------
Table 4. Pesticides and their major metabolites identified in some
of the poisoning cases and described in this report.
Oral LD Dermal LD
Pesticides Metabolites (mg/kg) (mg/kg)
A. Diethyl organophosphates - Alkyl Phosphates
Ethyl parathion DEP, DETP 3-33 21
Chlorpyrifos DEP, DETP 135 2,000
Dichlofenthion DEP, DETP 270 6,000
Diazinon DEP, DETP 100 - 150 900
B. Dimethyl organophosphates - Alkyl Phosphates
Mevinphos DMP 7 5-33
Methyl parathion DMP, DMTP 9-25 67
Dichlorvos (DDVP) DMP 56 - 80 75 - 107
Dimethoate DMP, DMTP, DMDTP 215
Naled (Dibrom) DMP 430 1,100
C. Organophosphates - Phenols
Ethyl, methyl parathion PNP
Chlorpyrifos 3,5,6-TCP
Dichlofenthion 2,4-DCP
D. Other pesticides - Phenols
Pentachlorophenol PCP 125 - 210
Carbaryl a naphthol 560 4,000
Lindane and its 2,4,6-TCP, 2,4,5-TCP,
isomers 2,3,4,6-TCP, 2,3,4,5-
TCP and 2,3,5-TCP 125
E. Organophosphate - Other Metabolites
Malathion MMA and MDA (majormeta- 1,000 - 4,000
bolites); DMP and 1,375
DMTP (minor metabolites)
LD s are based on animal studies
18
-------
SEQUENTIAL URINARY EXCRETION OF DIETHYL ALKYL PHOSPHATES IN FOUR FARM WORKERS
HOSPITALIZED DUE TO 10% ETHYL PARATHION GRANULAR DERMAL EXPOSURE
10.0
2.5
CB
a,
1.0
O.I
20 40 60
CASE #2
10.0
2.5
1.0
O.I
CASE #
2.5
1.0
O.I
0 20 40 60 0 20 40 60
HOURS AFTER HOSPITAL ADMISSION
CASE # 4
IOO
2.5
1.0
oDEP
• DETP
20 4X> 60
Figure 2
19
-------
SEQUENTIAL URINARY EXCRETIONS OF DIETHYL ALKYL PHOSPHATES IN THREE CASES OF POISONING
BY 6% ETHYL PARATHION MIXTURES DUE TO SPILLAGE OF THE CONCENTRATE
CASE #
1-2
8
4
CASE #
.8
66666666
HOUR am pm am pm am pm am pm
666 66666
am pm am pm am pm am pm
CASE # 7
2.4
1.6
.8
• DEP
o DETP
666666 6
am pm am pm am pm am
Figure 3
20
-------
Case #8
SEQUENTIAL EXCRETION OF DIALKYL PHOSPHATES AND
PHENOLIC METABOLITES FOLLOWING ACCIDENTAL ORAL
INGESTION OF DURSBAN IN A 3 YEAR OLD BLACK MALE
(L.W.)
• OEP
o OETP
6PM 6AM 6PM 6AM 6PM 6AM 6PM 6AM 6PM HOUR
HOSFftALIZEDt I ^2-PAM^
I ATROPINE 3.6 mg
50. -
4Q
20.
10.
3.5.6-TC PYRIDINOL
6PM 6AM 6PM 6AM 6PM 6AM 6PM 6AM 6PM HOUR
2/2/75 2/3/75 2/«»/75 2/5/75 2/6/75
Figure 4.
21
-------
Case #9
ug/ml
60
50
40
30
20
10
SEQUENTIAL EXCRETION OF DIALKYL PHOSPHATES AND
PHENOLIC METABOLITES FOLLOWING ACCIDENTAL ORAL
INGESTION OF DURSBAN IN A 3 YEAR OLD BLACK FEMALE
(A.J.)
• DEP
oDETP
12AM
MIDNIGHT
i
HOSPITALIZED
1
12AM 12AM
i 2
.1111
ATROPINE
12AM
-PAM
,,l 1
91.8 mg
12AM
1 |
12AM
1
t
12AM
40
30
20
3,5.6-TC PYRIDINOL
12AM 12AM 12AM
12AM 12AM 12AM
MIDNIGHT
3/24/79 3/25/75 3/26/75 3/27/75 3/28/75 3/29/75
Figure 5
22
-------
report last year (7). This organophosphate is highly soluble in adipose
tissue producing a slow release of the pesticide from the fat into the
circulation as serum concentrations shown in Figure 6 exemplify. The ex-
cretion pattern of the urinary alkyl phosphates from this pesticide are
shown in Figure 7 emphasizing the sensitivity of these indices to the body
burden of this pesticide, being still detectable in the urine for as long
as 80 days after exposure; this was also the same duration for identifying
the pesticide in serum. The DMP alkyl phosphate data shown in Figure 7
was possibly due to contamination of the dichlofenthion with a dimethyl
organophosphate.
b. Poisoning by dimethyl organophosphate' insecticides - Mevinphos
(Phosdrin) is the organophosphate in this group which most frequently
causes human poisonings; the major urinary metabolite is DMP. Urinary
metabolites were studied in three cases of poisoning by this insecticide
of which case number 11, shown in Figure 8 is a typical example. This
was a dermal exposure in a mixer-loader and the initial concentration of
DMP was 5 ug/ml, rose to 10 ug/ml in 8 hours and then was totally elimin-
ated 8 hours later.
c. Mixed diethyl and dimethyl poisoning - J.T., a 55 y/o w/m was
mixing and loading parathion 8E, toxaphene, dimethoate, and mevinphos
(Phosdrin). He developed serious cholinesterase illness and was hospi-
talized shortly thereafter with almost total cholinesterase inhibition.
The urine voided shortly after admission showed DMP 5»0 ug/ml; DMTP 0.8
ug/ml; DEP 0.7 ug/ml; DEP 1.5 ug/ml and DETP 3.3 ug/ml. These metabolites
illustrate the combined effects of phosdrin and ethyl parathion exposures,
demonstrating on the one hand the sensitivity of the index but emphasizing
on the other hand the lack of specificity of the index when exposures such
as these are mixed exposures.
d. Malathion poisoning - With malathion, the alkyl phosphates DMP,
DMTP, DMDTP are the minor metabolites and malathion mono-acid and malath-
ion di-acid being the major metabolites0 When a patient (case number 13)
ingested an unknown amount of 50% malathion, the initial concentration
of DMP was 2.5 ug/ml, DMTP was 87 ug/ml and interpretation of the DMDTP
was complicated by interfering peaks. It will be seen from Figure 9 that
the urinary excretion of malathion mono-acid and malathion di-acid was
very informative.
B. Discussion
Collectively these several poisoning case studies clearly demonstrate
the diagnostic potential of the urinary metabolites if the exposure has
been to a single pesticide. If additional phenolic metabolite data are
available, specific biologic information is obtained, permitting the pre-
cise identification of the material causing the cholinesterase illness.
With mixed pesticide poisonings, the situation is much more complex
23
-------
Figure 6. Serum concentrations of dichlofenthioh (ppb) and red cell
and plasma cholinesterase levels (^pH/hr) during recovery
following oral ingestion of dichlofenthion (VC-13)
_Q
Q.
^.
z
o
X
i—
Z
LLJ
U_
O
y
^^
0
O
}_
Q£
f~
u
z
o
u
ID
C£
UJ
CO
Case //10
180
160
140
120
100
80
60
40
20
0
-
• PLASMA
o RBC ChE
• VC 13 IN
_
0*
• *
" x- /
yl
'
1 1 1 ^»..
or> AC\ Lr\ t
80 100
DAYS POST POISONING
120
140
0.9
0.8
0.7
0.6
0.4
0.3
0.2
0.1
0
n
3-
0.5 P
c/>
T3
I
-------
Figure 7. Urinary excretions of alkyl phosphate metabolites of diehlo-
fenthion (VC-13) poisoning. Dade County, Fl. 1974
Case //10
10.0
1.0
0.1
.01
DEP
DETP
DMP
DMTP
20 40 60 80 100 120
DAYS POST POISONING
25
-------
Case ill-
SEQUENTIAL DMP EXCRETION (ufl/hrt IN A CASE OF
OCCUPATIONAL PHOSDRIN POISONING (DERMAL) IN A
39 YEAR OLD BLACK MALE (B.M.)
* DMP
HOUR
84 12 I 4 12 8 4 12 8 4 12 8 4 12 8
AM PM AM AM PM AM AM PM AM AM PH AM AM PM AM AM
2/12/75 2/13/75 2/14/75 2/15/75 2/16/75
Figure .8
26
-------
Case #12
Sequential excretion of malathion mono-acid (MMA) &
malathion di-acid (MOA) urinary metabolites following
oral ingestion of an unknown amount of malathion
concentrate
1000
100
E
a.
10
1.0
O.I
MMA
MOA
630 &30 &30 6=30 6'30 630 63O
pm pm pm pm pm pm pm
Figure 9
27
-------
because the urinary alkyl phosphates are group specific (diethyl and dimethyl
phosphates) but not pesticide specific. In these circumstances, the identi-
fication of the organophosphate group is facilitated but not the individual
pesticide. Similarly, from a quantitative point of view there are no absolute
concentrations of alkyl phosphates in the urine which can be considered
uniformly diagnostic of all organophosphate pesticides because the alkyl
phosphates are derived from organophosphates which have varying toxicities.
The several variables which influence the concentration of these metabolites
in the urine include: (1) the chemical configuration of the pesticide, (2)
its metabolism and toxicity, and (3) the dose and rate of exposure; the
dose and toxicity of the pesticide are the most important variables.
The ethyl parathion cases and the mevinphos case merit further dis-
cussion because these two pesticides are among the most toxic organophos-
phates being currently used by agriculture and are most often associated
with poisoning and/or severe cholinesterase inhibition. In the 7 cases
of parathion poisoning the lowest concentration of DEP observed in the
initial urine was 0.9 ug/ml with initial concentrations in all these cases
ranging from 0.9 to 8.1 ug/ml. These concentrations should be contrasted
with DEP concentrations observed in 99 urines from 8 workers primarily
exposed to these pesticides and found to have reasonably normal cholines-
terase levels. The average DEP concentration was 0.14 ug/ml and only on one
occasion was a DEP concentration greater than 0.4 ug/ml identified. Two
mevinphos cases were investigated and the initial urine concentration of
BMP was 5 ug/ml in both cases; these findings were very similar to those
reported by Holmes et al. (16) who found that initial urine concentrations
of DMP were 4.7 and 4.0 ug/ml respectively in two cases which they reported.
2, Occupational Exposure Studies with Urinary Alkyl Phosphate Excretions
a. Pesticide jLoader-mixer study - The objective of these urinary
metabolite studies was to measure the surveillance and predictive poten-
tial of these biologic indices in the occupational exposed worker con-
centrating in particular on the pesticide loader and mixer, whose pesti-
cide exposure is to a wide variety of chemicals. The work exposure of
two subjects, one of whom had a red blood cell cholinesterase of 0.60 A
pH/hr and a plasma cholinesterase of 0.50 ApH/hr (Worker A) and the other,
who had a red blood cell cholinesterase of 0.11 ApH/hr and a plasma cholin-
esterase of 0.10 ApH/hr, are shown in Table 5.
It will be noted that Worker A was exposed only to the dimethyl
organophosphate pesticides whereas Worker B besides sustaining a mixed
exposure to both diethyl and dimethyl organophosphate insecticides was
also exposed to pesticides which were far more toxic than those used
by Worker A.
Tables 6 and 7 and Figures 10 and 11 describe and illustrate the
sequential urinary excretion of pesticide metabolites during the 4 to
5 day work period of mixer loaders A and B. It should be noted that
although Worker A was exposed entirely to the DMP organophosphate pesti-
cides, the profile shows that he was sustaining small amounts of DEP
exposure whose source was unknown, emphasizing both the sensitivity of
the iadex and also the fact that in pesticide worker situations, unrecog-
nized 'exposures occur which are not described in the conventional work
28
-------
NJ
vO
Table 5. Pesticide exposure history of two aircraft mixer-
period of urinary alkyl phosphate surveillance.
loaders, before and during the
South Florida, 1975.
Period
Day before
Surveillance
Period
Day I
Day II
Day III
Day IV
Worker "A"
Alkyl phosphate
Pesticides mixed metabolites
Dimethoate (80%) DMP, DMTP, DMDTP
Dibrom (40%) DMP
Methomyl -
None - at home
Methomyl -
Methomyl -
Dimethoate (80%) DMP, DMTP, DMDTP
Dibrom (40%) DMP
Toxaphene
Worker "B"
Pesticides mixed
Dibrom (40%)
Diazinon
Dimethoate (80%)
Methomyl
Mevinphos (40%)
Dibrom (40%)
Parathion (8%)
Toxaphene
Dimethoate (80%)
Mevinphos (40%)
Diazinon
Dibrom (40%)
Alkyl phosphate
metabolites
DMP
DEP, DETP
DMP, DMTP,
- -
DMP
DMP
DEP , DETP
—
DMP, DMTP,
DMP
DEP, DETP
DMP
DMDTP
V
DMDTP
Day V
Methomyl
Mevinphos (40%) DMP
Dibrom . DMP
Ethyl parathion (6%) DEP, DETP
Methyl parathion (3%) DMP, DMTP
Dimethoate DMP, DMTP, DMDTP
Methomyl -
Toxaphene
-------
Table 6. Urinary alkyl phosphate metabolite studied in a mixer-loader (A) having
a normal cholinesterase level and whose pesticide exposure was to
dimethoate (Cygon) and dibrom. Belle Glade, Florida. 1975
Date
3/28/75
3/29/75
3/30/75
3/31/75
4/1/75
4/2/75
Hour
6:00 am
11:45 am
1:45 pm
6:05 pm
7:30 pm
10:20 pm
6:00 am
12 noon
2:20 pm
6:10 pm
10:00 pm
6:00 am
11:50 am
2:20 pm
9:15 pm
11:00 pm
6:00 am
11:50 am
6:10 pm
11:00 pm
6:15 am
12:15 pm
7:00 pm
11:00 pm
6:00 am
DMP
ug/ml
0.37
0.19
0.25
0.19
0.09
0.10
0.10
0.10
0.29
0.23
0.32
0.25
0.12
0.10
0.06
0.13
0.13
0.13
0.19
0.66
1.11
0.69
0.77 '
0.90
0.48
DMTP
ug/ml
0.33
0.49
0.10
0.16
0.80
0.22
0.21
0.21
0.17
0.20
0.18
0.15
0.11
0.29
0.32
0.21
0.30
0.19
0.17
1.13
0.92
0.58
1.06
0.96
0.36
DMDTP
ug/ml
0.04
0.02
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.04
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.04
0.03
0.04
0.17
0.19
0.03
0.10
0.11
0.12
DEP
ug/ml
0.11
0.07
0.09
0.07
N.D.
0.04
0.06
0.06
0.10
0.06
0.09
0.09
0.05
0.06
N.D.
0.07
0.05
0.05
0.06
0.09
0.18
0.12
0.15
0.19
0.17
DETP
ug/ml
0.10
0.07
N.D.
N.D.
N.D.
0.05
0.04
0.04
0.07
0.06
0.06
0.06
0.03
N.D.
0.06
0.04
0.08
N.D.
0.06
0.11
0.06
0.06
0.13
0.17
0.09
DEP _ .
DETP
1.1
1.0
0.0
0.0
0.0
0.8
1.5
1.5
1.4
1.0
1.5
1.5
1.6
0.0
0.0
1.7
0.6
0.0
1.0
0.8
3.0
2.0
1.1
1.1
1.8
*corrected for osmolality (800 ml/Osm/1)
N.D. = Not detectable
Limits of detectability for DMP 0.02 ug/ml;
DMTP 0.03 ug/ml; DMDTP 0.02 ug/ml; DEP 0-.03
ug/ml and DETP 0.02 ug/ml.
30
-------
Table 7. Urinary metabolite studies in a mixer-loader (B) having an inhibited
cholinesterase and whose work exposure was to a variety of pesticides.
Belle Glade, Florida. 1975
Date
4/21/75
4/22/75
4/23/75
4/24/75
4/25/75
Hour
3:50
6:45
3:00
5:30
6:20
9:35
9:05
11:15
2:45
6:30
7:30
9:30
5:30
9:45
12:00
2:00
2:15
4:55
5:30
7:30
9:40
10:00
2:55
7:30
7:45
6:05
10:30
11:30
pm
pm
am
am
am
am
pm
pm
am
am
am
am
pm
pm
am .
am
am
am
am
am
am
pm
am
am
am
pm
pm
pm
BMP
ug/ml
0.21
0.37
0.24
0.23
0.41
0.14
0.24
0.34
0.26
0.23
0.24
0.15
0.25
0.26
0.22
0.24
0.31
0.22
0.30
0.42
0.33
0.30
0.39
0.25
0.31
0.29
0.52
0.54
DMTP
ug/ml .
0.21
0.29
0.16
0.21
0.26
0.17
0.22
0.20
0.16
0.16
0.12
0.06
0.07
N.D.
0.29
0.26
0.26
0.21
0.20
N.D.
0.13
0.20
0.25
0.26
0.28
0.32
0.32
0.28
DMDTP
ug/ml
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.03
0.03
0.03
N.D.
DEP
ug/ml
0.11
0.10
0.11
0.14
0.18
0.07
0.30
0.40
0.37
0.26
0.37
0.24
0.41
0.24
0.17
0.14
0.20
0.14
0.18
0.28
0.24
0.21
0.27
0.18
0.24
0.20
0.20
0.15
DETP
ug/ml
0.10
0.15
0.27
0.28
0.12
0.09
0.31
0.50
0.14
0.19
0.13
0.06
0.15
0.12
0.15
0.27
0.16
0.16
0.35
0.15
0.10
0.39
0.12
0.12
0.16
0.14
0.19
0.12
PNP
ug/ml
1
1
1
0
0
0
1
1
1
0
0
0
0
1
0
0
0
0
0
0
0
0
0
0
0
0
0
0
.16
.19
.09
.98
.98
.58
.02
.70
.13
.90
.57
.53
.79
.01
.22
.34
.47
.43
.52
.38
.18
.64
.23
.22
.29
.23
.19
.06
DEP Ratio
DETP
1
0
0
0
1
0
1
0
2
1
2
4
2
2
1
0
1
0
0
1
2
0
2
1
1
1
1
1
.1
.6
.4
.5
.5
.7
.0
.8
.6
.4
.8
.0
.7
.0
.1
.5
.2
.8
.5
.8
.4
.5
.2
.5
.5
.4
.0
.2
N.D. = Not detectable
Limits of detectability are: DMP 0.02, DMTP 0.03, DMDTP 0.02,
DEP 0.02, DETP 0.02 and PNP 0.01.
31
-------
SEQUENTIAL EXCRETION OF URINARY ALKYL PHOS-
PHATES IN A MIXER LOADER (T.J.) WHOSE RED BLOOD
CELL CHOLINESTERASE WAS 0.60 A pH/HR. AND
PLASMA CHOLESTERASE 0.55 ApH/HR. DURING A
PESTICIDE EXPOSURE TO DIMETHOATE (CYGON) AND
DIBROM
1.30
1.10
.90
.70
.50
.30
.10
o DMDTP
• DMP VS. TIME
o DMTP '
TIMF 66666666666
i innt. Qfn pfp am pm am pm am pm am pm am
.10 ,
TlMF 666 66666666
1 II¥IQ am pm am pm am pm am pm am pm am
Figure 10
-------
SEQUENTIAL EXCRETION OF URINARY ALKYL PHOSPHATES
8 PARANITROPHENOL IN A MIXER-LOADER SJ.L.) WHOSE
RED BLOOD CELL CHOUNESTERASE WAS 0.11 ApH/HR. a
PLASMA CHOUNESTERASE 0.10 £pH/HR. DURING A
MIXED EXPOSURE TO PESTICIDES
2.50
1.90
1.70
1.50
o>
1. 10
.90
.70
.50
.30
.10
• DEP
o DETP
• PNP
VS. TIME
TIME 33333333333
Qfit piti cm put Qtn pm on pfn om pm oti\
.90
.50
.30
.10
oDMP
• DMTP
• DMDTP
TIME 3
cm
33
pin WR
3333
onn pin om pm
3. 3 3
cvn pm Qfn
Figure 11
33
-------
history study. Table 8 summarizes the mean and ranges of the alkyl phosphate
metabolite excretions from these two mixer-loaders; there is very little
difference in the average urinary excretion of the DMP in either worker
although the oxon-parent compound ratio was twice as high in Worker B
than in Worker A. There is however, a marked difference in the diethyl
metabolite concentrations, Worker B having 1^ times more mean concentrations
of DEP metabolites in his urine than what was found in Worker A. As
will be seen from Figure 11, DEP excretions in Worker B correlated in
time with the paranitrophenol (PNP) excretion indicating that the majority
of the DEP was coming from the ethyl parathion exposures suggesting that
it was this exposure to this toxic pesticide which was probably the major
reason for the cholinesterase differences in these two workers.
Because of the low cholinesterase finding observed in Worker B
and because several workers at this site were found to have severe cholines-
terase inhibition, a 24 hour air sample was collected at this work site
one month after the period of surveillance.1 The concentrations of pesti-
cides found in air (ng/m ) were as follows:
Diazinon 354
Malathion 24
Ethyl parathion 158
Methyl parathion 131
Mevinphos 4,650
Y BHC 1
Interfering peaks prevented the correct inter-
pretation of possible exposures of chlorpyrifos,
a BHC, heptachlor, aldrin, dieldrin, p,p' - DDT,
o,p' - DDT, endrin, a chlordane and y chlordane,
and toxaphene.
In addition, both mevinphos and methyl and ethyl parathion were
identified in a hexane wash extract of a T-shirt worn by one of the
mixer-loaders.
There were thus significant and unknown pesticide exposures occurring
at the work site where Worker B was employed, a finding which emphasizes
the limited interpretability which can be placed on the conventional
pesticide worker studies where exposure is entirely limited to pesticide
use information of the subjects under study. In this instance, the urinary
metabolite information and residue analyses showed that additional ex-
posures were occurring from pesticides in the air of the worker environ-
ment and in the worker's clothing. For comparison purposes, the mean
and ranges for the urinary alkyl phosphate excretions shown in Table 8
should be compared with the mean and ranges of these metabolites in 8
pilots and loaders also sustaining a mixed pesticide exposure which
included ethyl parathion but with normal cholinesterase levels (Table
7).
34
-------
•Table 8. Comparisons of mean and ranges, and ratios of urinary alkyl phosphate metabolites* (ug/ml)
in two mixer loaders found to have normal (A) and inhibited (B) cholinesterase levels.
Ratio
DMP Ratio
Subjects & No. study No. specimens DMP DMTP DMDTP DMTP + PEP DETP PEP
ChE levels/ days analyzed Tc and ranges x~ and ranges 3c and ranges PMPTP "x and ranges "x and ranges DETP
A 5 25 0.3 0.4 0.4 0.7 .08 .08 1.0
(.06 - .09) (.11 - .96) (ND** - .19) (NP - 0.19) (ND - 0.17)
RBC ChE 0.6
PI. ChE 0.55
JB 4 28 0.3 0.2 0.004 1.5 ^20 .18 1.17
(.14 - .54) (NP - .32) (NP - .03) (.1 - .41) (.06 - .50)
RBC ChE 0.10
PI. ChE 0.11
*corrected for osmolality of 800 ml/Osm/1
**Not detectable
•/ApH/hr - Michel method
-------
B. Discussion
Surveillance of the pesticide worker exposed to organophosphate and
carbamate insecticides is designed to detect and prevent serious cholin-
esterase inhibition and cholinergic illness. These are two human health
end points of special concern. In South Florida, past experience has
suggested that these effects are most likely to occur with workers working
with the more toxic pesticides such as parathion or mevinphos (17, 4, 3).
Sequential urinary metabolite studies which were conducted in the second
year of this project (6) showed that applicators working with relatively
non-toxic organophosphates such as chlorpyrifos, although exhibiting
significant urinary excretions of the alkyl phosphates of this pesticide
did not demonstrate simultaneous cholinesterase depression. Thus, the
the surveillance potential of this metabolite is of primary importance
only in situations where the worker is working with the more highly toxic
organophosphates. The findings presented in this study show that pre-
diction is impossible when the worker is exposed to a mixture of pesti-
cides, particularly when the mixture includes both highly toxic and rela-
tively nontoxic organophosphate pesticides.
Since today almost all agricultural practices call for the use of
a variety of organophosphate and carbamate insecticides, one must conclude
on the basis of these studies that although the urinary alkyl phosphate
metabolites are highly sensitive indicators of exposure to the organophos-
phates they do not hold much promise for being reliable non-specific pre-
dictors of cholinesterase depression in mixed exposure situations where
the pesticides involved differ greatly with regard to inherent toxicities.
This broad generalization of the potential of the urinary alkyl phosphates
as a surveillance instrument should be tempered by one clarification.
If in the future, occupational programs based upon metabolite excretions
are pursued, then standards might be set which would have to be based on
the worse theoretically possible situations, namely exposures to ethyl
parathion and mevinphos. One can envisage a situation where future occupa-
tional surveillance programs would be required only when workers were work-
ing with the more toxic pesticides. Under the circumstances, standards
for safe and unsafe levels of urinary alkyl phosphates could be set which
would be based on the metabolite concentrations observed with known expo-
sures to parathion and mevinphos. This biologic index would then become
a highly efficient surveillance instrument because safe and unsafe levels
would be based on single pesticide exposure to pesticides whose toxicity
was known.
A. Results
b. Urinary alkyl phosphate studies in workers exposed to foliar
residues - The objective of these studies was to test the evaluatory
potential of the urinary metabolites, imposing an intervention procedure
designed to produce subtle differences in exposure to foliar residues
in two groups of workers and to determine whether the urinary metabolites
were sensitive enough to detect these differences. Mean differences
in urinary alkyl phosphates between workers wearing fluorocarbon treated
36
-------
clothing and workers wearing untreated clothing are shown in Table 9.
The differences are the mean values of the untreated minus the treated
for twenty-four 12 hour urines collected over a six day study period.
For all four metabolites these differences were significant at the
p <.01 level. These showed that the workers wearing treated clothing
excreted significantly less amounts of urinary alkyl phosphates than workers
wearing untreated clothing. The significance of these differences was
the same whether the urinary metabolites were corrected or uncorrected
for osmolality. Tables lOa and lOb, and figures 12a and 12b also exhibit
striking temporal parallelism between excretion values of the two groups
further emphasizing the unique sensitivity of these indices.
B. Discussion
The above tables and figures demonstrate that the mean alkyl phos-
phate levels for each 12 hour urine period are higher in the untreated
group than in the treated group. This is true for 11 of 12 periods for
DMP and DEP, and 12 of 12 periods for DMTP and DETP. In addition, the
reliability of the urinary alkyl phosphate as an epidemiologic evaluatory
tool is amply demonstrated by these data, the sensitivity of these indices
readily permitting the identification of the different organophosphate
exposures of the two groups.
A. Results
3. Urinary alkyl phosphate studies in the general population
The objectives of these studies was to measure the profiles of inci-
dental exposure of a small sample of the general population of Dade
County to organophosphate and carbamate insecticides. Thus, Table 11
presents the mean, ranges and frequency of identification of the urinary
alkyl phosphate and phenolic metabolites in this Dade County general
population survey. The individual results are shown in Appendix A.
In an orange juice feeding study in which two volunteers participated
the orange juice had a DEP concentration of 0.01 ug/ml. Pre and post
cholinesterase determinations and urinary alkyl phosphates pre, during
and after drinking orange juice are shown in Table 12.
B. Discussion
Table 11 shows that there are minimal incidental exposure of the
general population in this area to trace amounts of organophosphates
and carbamates. Based upon a small sample size of 37 individuals between
36% and 56% of the population had trace amounts of organophosphates in
their urine and since 11 of these had trace amounts of 3,5,6-TCP this
would suggest that chlorpryifos was one major source of this incidental
organophosphate exposure. There was evidence of minimal incidental ex-
posure in 100% of the study sample to pentachlorophenol (PCP) and 27%
of the sample demonstrated small environmental exposure to chlorpyrifos
(Dursban).
37
-------
Table 9. Unadjusted and adjusted (for osmolar corrected) mean differences
in urinary alkyl phosphate levels between agricultural workers
wearing untreated and treated fluorocarbon clothing. 1975.
BMP DEP DMTP DETP
(ug/ml) (ug/ml) (ug/ml) (ug/ml)
A. Unadjusted
mean difference (over
12 hr time periods) .06 .05 .08 .04
standard error .015 .009 .007 .013
"p" <.01 <.01 <.01 <.01
B. Adjusted
mean difference (over
12 hr time periods) .06 .05 .06 .04
standard error .016 .009 .006 .012
"p" <.01 <.01 <.01 <.01
38
-------
OJ
VO
Table lOa. Comparison of the adjusted osmolar mean of twelve hour urinary alkyl phosphates (ug/ml) in workers
wearing untreated clothing and workers wearing fluorocarbon treated clothing over a six day period
Day
1
2
3
4
5
6
12 hour
urine
period
1
2
3
4
5
6
7
8
9
10
11
12
No.
subjects
11
11
11
12
12
12
11
11
11
10
11
10
V
Untreated
.05
.09
.11
.17
.38
.28
.26
.19
.22
.20
.23
.20
DMP (ug/ml)
No.
subjects
9
11
10
10
11
9
11
12
13
11
11
11
DEP (ug/ml)
X
Treated
.08
.07
.05
.11
.22
.15
.21
.19
.13
.15
.11
.19
mean difference=
standard
error=
A
Untreated-
Treated
-0.03
.02
.06
.06
.16
.13
.05
.00
.09
.05
.12
.01
.06
.016
X
Untreated
.11
.16
.15
.19
.31
.27
.27
.22
.21
.25
.25
.24
X
Treated
.12
.13
.09
.13
.25
.20
.21
.21
.16
.19
.13
.20
A
Untreated-
Treated
-0.01
.03
.06
.06
.06
.07
.06
.01
.05
.06
.12
.04
.05
.009
x = mean
A = difference
-------
Table lOb. Comparison of the adjusted osmolar mean of twelve hour urinary alkyl phosphates (ug/ml) in workers
"Airing untreated clothing and workers wearing fluorocarbon treated clothing over a six day period
weai
DMT.P (ug/ml)
Day
I
2
3
4
5
6
12 hour
urine
period
I
2
3
4
5
6
7
8
9
10
11
12
No.
subjects
11
11
11
12
12
12
11
11
11
10
11
10
X
Untreated
.07
.07
.11
.11
.17
.14
.24
.16
.21
.16
.15
.09
No.
subjects
9
11
10
10
11
9
11
12
13
11
11
11
X
Treated
.03
.04
.06
.03
.11
.05
.16
.13
.11
.15
.06
.05
mean difference=
standard error=
A
Untreated-
Treated
.04
.03
.05
.08
.06
.09
.08
.07
.10
.04
.09
.04
.06
.006
DETP (ug/ml)
"x
Untreated
.08
.05
.09
.08
.13
.13
.14
.10
.10
.12
.19
.12
X
Treated
.02
.05
.08
.04
.15
.06
.09
.07
.08
.09
.03
.04
A
Untreated-
Treated
.06
.00
.01
.04
.02
.07
.05
.03
.02
.03
.16
.08
.04
.012
x = mean
A = difference
-------
Comparison of mean urinary alkyl phosphates in workers
wearing fluorocarbon treated 8 untreated clothing
A
.3
.2
.1
0
.4
.3
.2
.1
0
12 hour
study periods
DMP
DEP
Treated
Untreated
8
10 12
day I day 2 day 3 day 4 day 5 day 6
lisure 12a
41
-------
.4
.3
.2
.1
0
.4
.3
.2
12 hour
study periods
Comparison of mean urinary akyl phosphates in workers
wearing fluorocarbon treated 8 untreated clothing
DMTP
DETP
Treated
Untreated
2 4 6 8 10 J2
day I day 2 day 3 day 4 day 5 day 6
Figure 12b
42
-------
Table 11. Mean and ranges and frequency of identification of alkyl phosphates and selected
phenols in the general population of Dade County, Florida, 1975
No. of
Metabolites subjects
A.
DMP
DEP
DMTP
DETP
B.
3,5,
PCP
2,4,
Alkyl Phosphates
36
36
33
33
Phenols
6-TCP 37
37
5-TCP 37
Mean
.008
.012
.027
.021
.003
.009
.004
Ranges
N.D. - .
N.D. - .
N.D. - .
N.D. - .
N.D. - .
.001 - .
N.D. - .
053
11
22
3
032
023
10
% Detected at or above limit of detectability
56%
58%
45%
36%
27%
100%
14%
-------
Table 12. Cholinesterase and urinary alkyl phosphate findings before, during, and after orange juice ingestion
Study
Phases
Pre-Orange
Juice
it
ii
ii
Orange Juice
n ii
ii ii
Post-Orange
Juice
ti ii
Date
12/15/76
ti
12/16/75
it
12/17/76
n
12/18/76
ti
12/19/76
ii
12/20/76
ti
12/21/76
n
RBC PI.
Sex ChE ChE
F
M
F 0.70 0.68
M 0.88 0.70
F
M
F
M
F 0.65 0.90
M 0.80 0.80
F
M
F
M
Vol.
Voided
250
750
250
780
1,165
750
870
1,550
1,200
1,230
340
310
600
ALKYL PHOSPHATES (ppm)
BMP
N.D.
N.D
N.D
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N-.D.
N-D.
N.D.
DMTP
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
DEP
N.D.
N.D.
N.D.
N.D.
N.D.
0.35
N.D.
0.05
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
DETP
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D. = Not detectable
-------
The orange juice study did not support the hypothesis of inciden-
tal organophosphate exposure from this dietary source.
4. Adipose pesticide residue studies in the occupationally exposed
A. Results
The objectives of these studies was (1) to determine whether any
fat soluble organophosphates had become part of the adipose pesticide
residue spectrum of the occupationally exposed worker, (2) to compare
simultaneous adipose and serum exposure of organochlorine pesticicdes
and (3) to measure urinary alkyl phosphate and phenolic metabolites in
pesticide formulations trying to relate these to worker histories and
air concentrations in the work environment. Table 13 presents the simul-
taneous adipose and serum concentrations of pesticides in five formulators.
Bromophos, a. fat soluble halogenated organophosphate insecticide was
identified in three of the samples analyzed. This is the first time
that a fat soluble organophosphate has been identified in persons occu-
pationally exposed to pesticides.
Although with only 5 subjects it is scarcely valid to attach
significance to the correlation of serum and fat levels, a bi-variate
Pearson correlation (18) was performed on adipose serum values. The
following correlations were demonstrated.
SERUM - FAT
COMPOUND CORRELATION COEFFICIENT (p)
a BHC 0.8856
$ BHC 0.9841
y BHC 0.7176
Heptachlor Epoxide 0.9895
Dieldrin 0.9037
p,p'-DDT 0.5373
p,p'-DDE 0.9906
Oxychlordane 0.9770
HCB 0.9789
Correlations of .9 or more were obtained from $ BHC, heptachlor epo-
xide, dieldrin, p,p'-DDE, oxychlordane and HCB when compared to serum
levels.
45
-------
Table 13. SIMULATANEOUS ADIPOSE AND SERUM CONCENTRATIONS OF PESTICIDES IN FIVE FORMULATORS. 1975.
Subject,
Initials and
years bf work
Expedience
A. P. b/m
18 years
fat (ppm)
serum (ppb)
J.P. w/m
15 years
fat (ppm)
serum (ppb)
T.W. b/m
3 years
fat (ppm)
serum (ppb)
J.T. b/m
3 years
fat (ppm)
serum (ppb)
E.W. b/m
4 months
fat (ppm)
serum (ppb)
Pesticides
Heptachlor
a-BHC
0.345
1.3
0.331
1.7
0.482
2.9
0.283
1.1
0.160
1.0
3-BHC
1.19
5.2
0.89
4.5
0.65
3.1
0.648
2.7
0.15
N.D.
Y-BHC A-BHC
0.268 0.035
0.97
0.315 0.100
1.9
0.436 0.166
1.6
0.168 0.038
1.0
0.142 0.036
1.0
epoxide
2.44
11.8
2.91
12.6
3.89
19.3
1.33
5.4
0.39
2.6
Dieldrin
0.542
3.7
0.680
4.6
0.724
4.5
0.407
N.D.
0.148
N.D.
P,p'-DDT
3.35
7.1
2.56
6.2
1.05
6.2
2.23
5.8
1.36
N.D.
o.p'-DDT
0.145
N.D.
0.162
N.D.
0.131
N.D.
N.D.
N.D.
0.2
N.D.
p , p-DDE
21.6
70.1
11.8
37.6
4.78
15.4
11.06
38.3
14.54
53.4
Total
DDT
27.5
85.2
17.3
48.1
13.0
23.4
14.6
48.5
17.7
59.5
Oxy-
chlor
dane
2.45
6.1
1.15
3.5
0.49
1.9
0.23
N.D.
0.14
N.D.
HCB
0.612
5.3
0.232
2.3
0.141
1.9
0.108
1.0
0.05
N.D.
Bromo-
phos
0.03
N.D.
0.02
N.D.
0.04
N.D.
N.D.
N.D.
N.D.
N.D.
-------
Table 14 presents cholinesterase and urinary alkyl phosphate concentra-
tions in these five femulators. The pesticides which were being formulated
during the week that these specimens were collected were: chlorpyrifos,
DDVP, carbaryl, sulphur, BHC, toxaphene, chlordane, dithane and M-45.
Two 24 hour air samples were collected inside the formulating plant. The
first was collected five months before the fat biopsy was obtained and
the other one month after the collection of the fat biopsy. The concentra-
tions of the pesticides in air are shown below:
Chlorpyrifos
Diazinon
Malathion
a BHC
Heptachlor
Aldrin
y BHC
Dieldrin
p,p'-DDT
o,p'-DDT
Endrin
Ethyl parathion
Methyl parathion
Methyl bromophos
Mevinphos
a chlordane
Y chlordane
Phorate
HCB
Ronnel
B. Discussion
•j
Sample #14 (ng/m )
June 11-12, 1975
168
470
170
3,977
7,315
655
4,791
88
73
43
43
86
182
4,130
8
432
2,328
N.D.
N.D.
N.D.
Sample #29 (ng/m )
December 12-13. 1975
65
168
9
2,301
25,243
N.D.
3,779
24
N.D.
N.D.
N.D.
17
Interference
1,715
Interference
597
3,068
1
387
2
When one looks at the pesticides being handled by these femulators,
and the air concentrations of pesticides detected inside the plant and tries
to relate these to the epidemiologic information provided by adipose and urine
metabolite studies, it is obvious that these two biologic indices reflect
recent exposures, expressed by the urine data and long term exposures
reflected by the adipose data. As may be expected, the organochlorine
residues are significantly higher than those seen in the general popu-
lation, and although many of the pesticides identified in the adipose
residues have not been formulated recently, their presence in the fat
almost certainly reflects the persistent exposure to these chemicals
through concentrations in air. Total DDT levels in fat correlated well
with person years of employment in the plant but this association was
not so constant with the other organochlorine pesticides detected. The
recognition of bromophos (an organophosphate of low toxicity) in the
47
-------
-p-
oo
Table 14- SIMULTANEOUS CHOLINESTERASE AND URINARY ALKYL PHOSPHATE AND PHENOLIC METABOLITES OF
PESTICIDES IN FIVE FORMULATORS. DADE COUNTY, FLORIDA. 1975
Initials and
years of work
experience
A. P. b/m
18 years
J . P . w/m
15 years
T.W. b/m
3 years
J.T. b/m
3 years
E.W. b/m
4 months
RBC
ChE*
(ApH/hr)
0.89
0.70
0.70
0.57
0.80
PI.
ChE*
(ApH/hr)
0.35
0.41
0.27
0.55
0.50
Alkyl
BMP
0.07
0.01
N.D.
0.08
0.04
phosphates (ug/ml)
DMTP
0.13
0.04
N.D.
N.D.
N.D.
DEP DETP
0.06 N.D.
0.08 N.D.
0.05 N.D.
0.04 N.D.
0.08 N.D.
PCP
0.016
0.010
0.006
0.032
0.012
235-
*• > J » ->
TCP
0.24
0.11
0.12
0.14
0.18
Phenol
(ug/ml)/
4-bromo-
2,5
DCP
0.32
0.20
0.07
0.09
0.07
2,4,6-
TCP
0.04
0.04
0.02
0.04
0.02
2,3,
4,6,
TTCP
0.02
0.01
0.01
0.01
0.004
2,3,
5,6,
TTCP
0.002
N.D.
N.D.
0.002
N.D.
/We were not able to calculate 2,4,5-TCP and 2,3,5-TCP because they had the same retention time in
three different columns (4% SE30-6% QF-1), (1.5% OV17-1.95% QF-1), (5% OV-210).
*Michel method
N.D. = Not detectable
-------
fat of these workers merely adds the added dimension of persistence to
some of the newer and less polar organophosphates now coming on the market
and emphasizes the need for additional evaluation of this property and
the consequences of these properties for man and his environment.
With regard to the urinary metabolite findings of PCP concentrations,
these were of an order of magnitude similar to that found in the
general population, suggesting that this exposure was incidental rather
than occupational. The urinary alkyl phosphate findings as well as the
red blood cell cholinesterase levels were generally reassuring suggest-
ing that the occupational health and safety practices in this plant
were sufficient to prevent significant human exposures to the organo-
phosphate insecticides, 3,5,6-trichloropyridinol data was indicative
of occupational chlorpyrifos exposures since these concentrations were
greater than those found in the general population.
5. Pesticide residue studies in the general population
A. Results
The objectives of these studies were (1) to determine whether any
of the less polar organophosphates formed any part of the adipose pesti-
cide residue spectrum of the general population, and (2) to compare the
prevalence of organochlorine pesticides in the 1975 sample with the levels
observed in the earlier surveys. The individual results are shown in
Appendix B.
No organophosphate pesticide residues were detected in this small
sample of the general population. The arithmetic mean and standard
deviation and ranges of eight organochlorine pesticides identified in
the adipose tissue are shown in Table 15. These levels are compared
with the levels found in 1970 (Table 15). Oxychlordane and HCB were
not identified in earlier surveys.
Figures 13a and 13b illustrate the frequency distribution of Total
DDT, oxychlordane, HCB, BHC, heptachlor epoxide and dieldrin residues
in this small sample.
6. Pesticide Air Sampling Studies
A. Results
The objectives of these studies were to continue monitoring air
concentrations of pesticides in the several sites described earlier.
Emphasis was placed on (1) the Everglades, (2) Miami suburbs, (3)
downtown Miami (Miami International Airport) and (4) a community health
center located one mile north of a formulating plant (South Dade Community
Health Center). The individual concentrations of pesticides in air in
the urban and suburban samples collected and analyzed are shown in Table
16. Work site studies are shown in Table 17; these are air concentrations
of pesticides at two crop dusting sites and two samples collected inside
a formulating plant. The data collected on all 40 samples are shown in
Appendix C.
49
-------
Table'15. COMPARISON OF ADIPOSE ORGANOCHLORINE PESTICIDE RESIDUES
(PPM) IN DADE COUNTY GENERAL POPULATION (ADULTS).
1975 AND 1970.
Pesticides
p,p'-DDT
p , p ' -DDE
Total DDT
Dieldrin
Oxychlordane
HCB
B BHC
Heptachlor
Epoxide
Year
1975
1970
1975
1970
1975
1970
1975
1970
1975
1975
1975
1970
1975
1970
Number
20
122
20
122
20
122
20
122
20
20
20
122
20
122
Mean
0.9
1.6
5.8
5.6
7.5
7.8
0.2
0.3
0.1
0.1
0.2
0.3
0.1
0.1
Standard Deviation Ranges
0.8
1.6
3.7
4.0
4.7
5.7
0.2
0.3
0.1
0.1
0.2
0.2
6.02
0.05
0.11 -
0.01 -
1.00 -
0.05 -
1.43 -
0.01 -
0.02 -
.005 -
0.05 -
0.02 -
0.08 -
N.D. -
0.03 -
N.D. -
3.1
13.0
11.5
21.0
14.3
28.6
0.7
2.2
0.3
0.4
0.6
1.4
0.1
2.7
50
-------
Figure 13a. Frequency distribution of organochlorine residues in
adipose tissue of the Dade County general population.
1975.
B BHC (ppm) IN ADIPOSE TISSUE (wet wt.)
N= 20
Geometric mean = .162
Median = .156
.02- Q4- O8- .16- .32-
.039 079 .159 .319 .639
2. HEPTACHLOR EPOXIDE (ppm)
N r 19
Geometric mean = .053
Median = 0.53
.02- .03- .04- .05- .06- .07- .08- .09- .10-
.029 .039 049 O59 O69 .079 O89 O99 .109
3. DIELDRIN (ppm)
N = 20
Geometric means.114
Median = .103
.01- .02- .04- .08- .16- 32- .64-
.019 039 .079 J59 319 639 1279
51
-------
Figure 13b. Frequency distribution of organochlorine residues in
adipose tissue of the Bade County general population.
4. TOTAL DOT (ppm) IN ADIPOSE TISSUE (wet wt.)
N = 20
Geometric mean = 5.83
Median = 6.25
I- 3- 5- 7- 9 II 13
Z9 4.9 6.9 89 10.9 129 14.9
5- OXYCHLORDANE (ppm) IN ADIPOSE TISSUE (wet wt.)
N =20
Geometric mean = .103
Median = .09
.03- .06- J09- J2- .15- J8- .21- .24- .27- .30- .33- .36- .39-
.099 D89 .119 .(49 .179 209 .239 .269 .299 .329 .359 .389 .419
6 "CB (ppm) IN ADIPOSE TISSUE (wet wt.)
Geometric mean = .048
Median = .051
.0- JDS- 06- J09- 12- .15- J8- 21- .24- 27- .30- 33- 36-
.029 J059 J089 .119 .149 .179 209 239 269299.329 359 .389
52
-------
Table 16. Medians and ranges of air concentrations (ng/m ) of pesticides observed in
locations with repeated air sampling surveys. South Florida 1975-76.
Pesticide and
Their Limits
of Detectability
Suburban Site
(17 samples)
MecL. Ranges
Airport Site
(8 samples)
Med. Ranges
So. Bade Connn.
Hlth Ctr (9 samples)
Med . Ranges
Everglades
(2 samples)
Ranges
Dichlofenthion
Chlorpyrifos
Diazinon
Malathion
a BHC
Heptachlor
ATdrin
Y BHC
Dieldrin
Mevinphos
a Chlordane
Y Chlordane
(0.2)
(0.3)
(0.2)
(1.0)
(0.1)
(0.1)
(0.2)
(0.1)
(0.3)
(0.5)
(0.2)
(0.3)
N.D.*
1.0
1.5
N.D.
0.3
8.7
N.D.
0.3
0.3
N.
0.6
1.0
N.D. - 1.4
0.3 - 11.5
N.D. - 17.6
N.D. - 9.2
0.1 - 1.5
0.34 - 8.7
N.D. - 0.47
N.D. - 1.3
N.D. - 1.0
D.
0.3 - 3.0
0.41 - 12.7
.75
1.1
N.D.
0.3
0.75
0.16
0.18
N.D.
0.41
0.8
N.D.
N.D. -
N.D. -
N.D. -
0.1 -
0.35 -
N.D.
N.D. -
N.D. -
N.D. -
0.16 -
0.3 -
N.D. N.D.
22.3 0.8 N.D. - 1.6 N.D.
5.9 0.8 N.D. - 5.4 N.D. - 3.2
6 N.D. N.D. - 7.2 N.D.
0.9 0.3 N.D. - 2.2 0.1 - 0.5
3.64 1.0 0.64 - 3.9 0.22 - 0.7
N.D. N.D.
0.6 0.4 N.D. - 1.0 N.D. - 0.1
0.3 0.3 N.D. - 0.7 N.D.
3.0 N.D. N.D.
0.9 0.3 0.15 - 1.2 N.D. -.0.2
2.0 0.9 0.12 - 2.2 N.D. - 0.7
N.D. = Not detectable
All the following pesticides were not detected in any of the samplings: p,p'-DDT, o,p'-DDT, endrin, ethyl parathion, methyl
parathion, methyl bromophos, phorate, HCB, A BHC, Endosulfan I, Ronnel, Toxa-
phene, ethion.
-------
Table 17. Air concentrations (ng/m ) of pesticides and their ranges at four occupational work sites in
South Florida, 1975.
Pesticides
Chlorpyrifos
Diazinon
Malathion
yBHC
Heptachlor
Aid r in
YBHC
Dieldrin
p , p ' -DDT
o,p'-DDT
End r in
Ethion
Ethyl Parathion
Methyl Parathion
Methyl Bromophos
Mevinphos
Phorate
HCB
YChlordane
YChlordane
ABHC
Endosulfan
Ronnel
Toxaphene
Sample (m^)
South Dade
Crop Dusting
3/20-21/75
0.20
3.23
N.D.
1.5
1.1
N.D.
3.5
1.0
N.D.
N.D.
3.3
1.1
7.6
4.5
N.D.
N.D.
N.D.
N.D.
1.6.
2.7
N.D.
6.3
N.D.
N.D.
41.5
Belle Glade
Crop Dusting
5/19-20/75
I
354
24
I
I
I
1.0
I
I
I
I
N.D.
158
131
N.D.
4,650
N.D.
N.D.
I
I
N.D.
N.D.
N.D.
Present
50
Inside Formulation Inside Formulation
Plant Plant Ranges of
6/11-12/75 12/12-13/75 Four Work Sites
168
470
170
3,977
7,315
655
4,791
88
73
43
19
N.D.
86
182
4,130
9
N.D.
N.D.
432
2,328
N.D.
N.D.
N.D.
N.D.
52
65
168
9
2,301
25,243
N.D.
3,779
24
N.D,
N.D.
N.D.
N.D.
17
I
1,715
I
1
387
597
3,068
1,141
N.D.
2
N.D.
47.4
0.2 -
3.2 -
N.D.-
1.5 -
1.1 -
N.D.-
1.0 -
1.0 -
N.D.-
N.D.-
N.D.-
N.D.-
7.6 -
4.5 -
N.D.-
N.D.-
N.D.-
N.D.-
1.6 -
2.7 -
N.D.-
N.D.-
N.D.-
168
470
170
3,977
25,243
655
4,791
88
73
43
19
1.1
158
182
4,130
4,650
1
387
597
3,068
1,141
6.3
2
Present
N.D. = Not detectable
I = Interfering peaks caused by Toxaphene
-------
B. Discussion
The major source of air contamination in South Florida is from
areas where pesticides are indiscriminately mixed and loaded in the fields
and. inside pesticide formulating plants. General concentrations of
pesticides in the ambient air from agriculture and horticulture use and
in an area in close proximity of the formulating plant, were minimal.
Recently it has been proposed and approved by the Environmental
Protection Council of Dade County to resort to open-air burning of
pesticide containers. Previously, containers were disposed by des-
truction and burial. This procedure has been thought to threaten the
water table resources of South Florida and because of a sizeable buildup
of used containers in this area, the alternative solution of open-air
burning has been approved for a period of six months. In the light of
the air monitoring data presented in this report and in the light of
this decision to resort to open-air burning, it seems to be imperative
that the effect of this new method of air dispersal in this area should
be monitored for the future.
Finally, DDT has disappeared, except for inside the formulating
•plant. Malathion is detectable only during the mosquito control programs,
and dichlofenthion, commensurate with no further production of this product,
is no longer found in the suburban air sampling site.
55
-------
REFERENCES
1. Davies, J.E. Pesticides and the Environment. A Review of the
Changing Profile of Pesticides' Effect on Human Health. Boletin
de la Oficina Sanitaria Panamerican (English edition). 6(3):24,
1972.
2. Reich, G.A., Davis, J.H.. and Davies, J.E. Pesticide Poisoning
in South Florida: An analysis of mortality and morbidity and a
comparison of sources of incidence data. Arch. Environ. Health
17:768, 1968.
3. MacDonald, W.E. and Deichman, W.B. Pesticides Used in Dade County,
Florida during 1962. PESTICIDE SYMPOSIA, W.B. Deichman, Ed.,
Halos and Associates Inc., Miami, 1972.
4. Davies, J.E. Pesticide Residues in Man. ENVIRONMENTAL POLLUTION
BY PESTICIDES, C.A. Edwards, Editor. Plenum Press, London, 1973.
5. Davies, J.E. Pesticides Epidemiological Field Studies. Environ-
mental Health Effects Research Series. EPA-650/1-74-009. Office
of Research and Development, U.S. Environmental Protection Agency,
Washington, D.C., 1974.
6. Davies, J.E. Occupational and Environmental Pesticide Exposure
Study in South Florida. Environmental Health Effects Research
Series. EPA-650/1-75-002. Office of Research and Development.
U. S. Environmental Protection Agency, Washington, D.C., 1975.
7. Davies, J.E., Barquet, A., Freed, V.H., Haque, R., Morgade, C.,
Sonneborn, R.E., Vaclavek, C. Human Pesticide Poisonings by Fat-
Soluble Organophosphate Insecticide. Arch, of Environ. Health
30(12):608,.1975.
8. Davies, J.E., Freed, V., Briese, F.W., Shafik, T.M., Astascio, N.,
People, A. The Protection of Pesticide Exposure of Agricultural
Workers. (Abstract) 104th Ann. Mtg. of the Amer. Public Health
Assn., Oct. 17-21, 1976, Miami Beach, Fl.
9. Fiske Osmometer Manual. Fiske Associates Inc., 1962.
10. Shafik, T.M., Bradway, D., Enos, H., Yobs, A. Human Exposure to
Organophosphorus Pesticides: A Modified Procedure for Gas Liquid
Chromatographic Analysis of Alkyl Phosphate Metabolites in Urine.
J. Agr. Fd. Chem. 21:625, 1973.
11. Shafik, T.M., Sullivan, H.C., Enos, H.F. A Multiresidue Procedure
for Halo and Nitrophenols - Measurement of Exposure to Biodegradable
Pesticides Yielding These Compounds as Metabolites. J. Agr. Fd.
Chem. 21:295, 1973.
12. Shafik, M.T. and Bradway, D. Malathion Exposure Studies. The Deter-
mination of Mono- and Dicarboxylic Acids and Alkyl Phosphates in
Urine. Presented at the 161 Amer. Chem. Soc., Los Angeles, Cal.
March 28-April 2, 1971.
-------
References - Continued
13. Michel, H. An Electrometric Method for the Determination of Red
Blood Cell and Plasma Cholinesterase Activity. J. Lab. Clin.
Med. 34:1564, 1949.
14. Sherma, J. and Shafik, T.M. A Multiclass, Multiresidue Analytical
Method for Determining Pesticide Residues in Air. Arch. Environ.
Contain. & Toxicol. 3:55, 1975.
15. Pesticide Analytical Manual - F.D.A., 1967 (Yearly Revision).
Office of the Associated Commissioner for Compliance. Rockville,
Maryland, 1967.
16. Holmes, J.H., Starr Jr., H.G., Hanisch, R.C., Von Kaulia, K.N.
Short-Term Toxicity of Mevinphos in Man.
57
-------
BIBLIOGRAPHY
Davies, J.E. and W. F. Edmundson. Epidemiology of DDT. Futura
Publishing Company, Inc., Mount Kisco, New York, 1972.
Deichman, W.B. Pesticides and the Environment: A Continuing
Controversy. Intercontinental Medical Book, Corp., New York
New York, 1973.
Edwards, C.A. Environmental Pollution by Pesticides. Plenum
Press, New York, New York, 1973.
Gunther, F.A. and J.D. Gunther. Residue Reviews. Springer-
Verlag, New York, New York, 1976.
Hamilton, A. and H.L. Hardy. Industrial Toxicology. Publishing
Sciences Group, Inc., Acton, Massachusetts, 1974.
Kay, K., M. M. Hipskind, and M. Schafer, et al. Adverse Effects
of Common Environmental Pollutants. MSS Information Corp.,
New York, New York, 1972.
Report of the Secretary's Commission on Pesticides and Their Relation-
ship to Environmental Health. Parts I and II. U.S. Department
of Health, Education & Welfare. U. S. Government Printing Office,
Washington, D.C., 1965.
58
-------
APPENDICES
A. General Population Raw Data
B. Adipose Pesticide Residue Raw Data
C. Air Monitoring Raw Data
59
-------
Appendix A. Urinary metabolite concentrations in grab sample urines from 40 members of the
general population in South Florida. 1975
Age
& Sex
32/f
69/f
23/m
23/f
74/f
28/f
4/m
35/m
46/m
10/m
42/f
39/m
49/f
36/m
32/f
24/f
40/m
21/m
55/m
51/m
33/m
26/m
21/f
29/m
19/f
48/m
16/m
21/m
50/f
36/m
45/m
23/f
It
38/f
49/f
53/m
50/m
72/m
4%/m
51/f
T'll"1 •*•'«! Ill •""•
ALKYL PHOSPHATE (ug/ml)
Occupation
Cashier
Housewife
Lab Technician
Secretary
Housewife
Housewife
Adolescent
Hairdresser
Draftsman
Student
Seamstress
Asst. Professor
Counselor
Manager
Secretary
Lab Technician
Lab Supervisor
Mail Clerk
Mail Supervisor
College Professor
Lab Technician
Airplane Mech.
Secretary
Lab Techician
Secretary
Unemployed Lab.
Unemployed
Lab Technician
. Reg. Nurse
Reg. Nurse
Plasterer
Packing Clerk
Housewife
Chemist
Chemist
Physician
Investigator
Retired
Adolescent
Housewife
DMP
0.053
0.010
0.040
0.29
0.011
0.010
0.008
0.023
N.D.
N.D.
0.003
0.003
0.004
0.005
N.D.
0.010
N.D.
N.D.
N.D.
N.D.
N.D.
0.009
0.007
0.010
N.D.
0.012
0.024
0.017
N.D.
N.D.
0.007
N.D.
N.D.
N.D.
N.D.
0.03
N.D.
0.03
0.03
N.D.
DMTP
0.
0.
0.
0.
0.
0.
N.
0.
N.
N.
0.
N.
0.
N.
N.
0.
0.
N.
N,
N.
N.
N.
0.
0.
N.
N.
N.
N.
N.
N.
N.
N.
N.
0.
0.
0.
0.
0.
0.
0.
22
040
075
024
021
018
D.
034
D.
D.
012
D.
015
D.
D.
027
035
D.
D.
D.
D.
D.
026
027
D.
D.
D.
D.
D.
D.
D.
D.
D.
08
04
04
16
08
04
04
DEP
0.11
0.008
0.043
0.021
0.012
0.021
0.021
0.010
N.D.
N.D.
0.015
0.08
0.010
0.007
N.D.
0.019
N.D.
0.006
N.D.
N.D.
N.D.
0.011
0.006
0.007
N.D.
0.013
0.016
0.005
0.028
N.D.
0.027
N.D.
N.D.
0.04
N.D.
0.04
N.D.
0.04
0.04
N.D.
DETP
0.
0.
0.
0.
0.
N.
N.
N.
N.
N.
0.
N.
N.
N.
N,
0.
N.
0.
0.
N.
N.
N.
0.
0.
N.
N.
N.
N.
N.
N.
N.
N.
N.
0,
N.
0.
0.
0.
0.
0.
022
021
037
037
021
D.
D.
D.
D.
D.
030
D.
D.
D.
D.
042
D.
033
030
D.
D.
D.
029
019
D.
D.
D.
D.
D.
D.
D.
D.
D.
04
D.
073
05
3
04
04
3,5,6-TCP
0.006
N.D.
N.D.
N.D.
0.006
N.D.
N.D.
N.D.
N.D.
N.D.
0.008
0.008
0.024
0.006
N.D.
N.D.
N.D.
0.032
N.D.
N.D.
N.D.
N.D.
N.D.
0.006
N.D.
N.D.
N.D.
0.008
N.D.
N.D.
0.002
N.D.
N.D.
0.008
N.D.
N.D.
Not Done
N.D.
Not Done
Not Done
PHENOLS (ug/ml)
PCP
0.016
0.002
0.004
0.032
0.004
0.020
0.016
0.022
0.016
0.004
0.006
0.010
0.010
0.012
0.010
0.008
0.002
0.006
0.004
0.006
0.001
0.012
0.010
0.006
0.006
0.006
0.020
0.006
0.002
0.002
0.006
0.023
0.002
0.016
0.015
0.008
Not done
0.009
Not done
Not done
2,4,5-TCP
N.
N.
N.
N.
N.
N,
N.
N.
N.
N.
0.
N.
N.
N.
N.
N.
0.
N.
N.
N.
N.
0.
N.
N.
N.
N.
0.
N.
N.
N.
N.
N.
N.
N.
0.
N.
Not
N.
Not
Not
D.
D.
D.
D.
D.
D.
D.
D.
D.
D.
1
D* •
D.
D.
D.
D.
014
D.
D.
D.
D.
004
D.
D.
D.
D.
004
D.
D.
D.
D.
D.
D.
D.
04
D.
done
D.
done
done - -'
Not detected
-------
Appendix B= Individual levels of organochlorine and organophosphorus pesticide residues in adipose
tissue from 20 patients coming to surgery in a local hospital. Dade County, 1975
Maine
M.R.
M.L.
F.T.
J.O.
O.M.
A.D.
E.N.
W.P.
P.M.
C.H.
C.H.
A.G.
X.A.
G.C.
R.E.
J.H.
C.M.
P.S.
B.B.
C.E.
Age, race
and sex
19 y/o wm
38 y/o wf
33 y/o bf
48 y/o bf
23 y/o bm
34 y/o wm
50 y/o wm
65 y/o bm
64 y/o wm
70 y/o wm
67 y/o wf
52 y/o wf
39 y/o wf
51 y/o bf
77 y/o bf
47 y/o wf
35 y/o bf
43 y/o wf
22 y/o wf
32 y/o bf
p,p'-DDT
ppm
0.11
3.05
1.90
0.82
0.45
0.53
0.53
1.02
0.64
0.35
1.12
0.47
0.72
0.20
0.74
2.43
1.56
0.32
0.40
1.13
p,p'-DDE
ppm
1.04
9.94
9.39
8.59
11.20
2.81
3.70
6.41
4.72
2.12
8.92
2.57
3.46
1.00
10.15
9.33
4.28
1.02
3.31
11.46
o,p'-DDT
ppm
N.D.
0.15
N.D.
Inter.
0.24
0.11
N.D.
0.18
0.12
0.97
0.09
0.06
0.26
0.11
0.64
0.22
0.18
0.12
0.33
0.33
Total DDT
ppm
1.27
14.25
12.35
10.39
13.16
3.77
4.65
8.34
6.00
2.80
11.13
3.38
4.82
1.43
12.69
13.03
6.50
1.57
4.40
14.22
Oxychlor-
dane ppm
0.072
0.136
0.050
0.205
0.065
0.103
0.390
0.281
0.280
0.138
0.122
0.092
0.080
0.087
0.058
0.084
0.103
0.037
0.046
0.096
HCB
ppm
0.07
0.11
0.06
0.05
0.02
0.04
0.02
0.06
0.09
0.08
0.08
0.02
0.06
0.03
0.07
0.06
0.03
0.03
0.05
0.02
B-BHC
ppm
0.03
0.23
0.10
0.35
0.04
0.15
0.08
0.30
0.17
0.10
0.62
0.14
0.11
0.16
0.15
0.25
0.21
0.11
0.36
0.02
Hep.
Epox.
0.04
0.05
0.03
0.05
0.07
0.07
Inter.
0.08
0.10
0.11
0.03
0.06
0.08
0.04
0.04
0.04
0.05
0.04
0.27
0.49
Dieldrin
ppm
0.08
0.07
0.20
0.10
0.04
0.27
0.05
0.47
0.08
0.11
0.06
0.02
0.67
0.06
0.11
0.37
0.17
0.08
0.05
0.07
OP
PJBffi
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D. - Not detectable
Limits of detectability are: p,p'-DDT 0.09, p,p'-DDE 0.034, o,p'-DDT 0.081, oxychlordane 0.018, HCB 0.008,
B BHC 0.015, heptachlor epoxide 0.011 and dieldrin 0.017.
Inter. - Interference, unable to calculate
-------
Appendix C-l.
NJ
Concentrations of pesticides (ng/m ) in air samples collected from several sites in
South Florida 1975 - 1976
Pesticide
Dichlof enthion
Chlorpyrifos
Diazinon
Malathion
a BHC
Heptachlor
Aldrin
y BHC
Dieldrin
Endrin
Ethion
Ethyl Parathion
Methyl Parathion
a Chlordane
Y Chlordane
Endosulfan I
m3
Air #1
ng/m-3
N.D.
N.D.
3.2
N.D.
0.10
0.22
N.D.
0.1
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
37.2
Location Everglades
Wind-Start
Finish
Date Collected
E-NE
E.
2/11-12
Air #2
ng/m3
0.22
3.10
2.9
N.D.
0.24
1.3
0.47
0.26
0.49
N.D.
N.D.
N.D.
N.D.
0.36
1.2
N.D.
50.9
Suburban
Calm
E
2/11/12
Air #3
ng/m3
N.D.
0.72
3.3
N.D.
0.16
0.42
N.D.
0.1
0.16
N.D.
N.D.
N.D.
N.D.
0.16
0.49
N.D.
51.7
Airport
W
E
2/12-14
Air #4
ng/m3
N.D.
0.20
3.23
N.D.
1.5
1.1
N.D.
3.5
1.0
3.3
1.1
7.6
4.5
1.6
2.7
6.3
41.5
Tri-State
Calm
E
3/20-21
Air #5
ng/m3
N.D.
0.3
1.1
N.D.
0.6
1.2
N.D.
0.6
0.2
N.D.
N.D.
N.D.
N.D.
0.3
0.5
N.D.
53
SDCHC
NE
Calm
3/21-22
Air #6
ng/m3
0.3
0.5
1.9
N.D.
0.3
1.2
N.D.
0.4
0.3
N.D.
N.D.
N.D.
N.D.
0.7
1.0
N.D.
54
Suburban
SE
S-SE
4/9-10
Air #7
ng/m3
N.D.
N.D.
1.5
N.D.
0.4
0.9
N.D.
0.3
N.D.
N.D.
N.D.
N.D.
N.D.
0.5
0.7
N.D.
36
Airport
S-SE
S
4/9-10
Air #8
ng/m3
N.D.
1.6
3.0
. 7.2
0.7
0.8
N.D.
0.5
0.4
N.D.
N.D.
N.D.
N.D.
1.1
0.9
N.D.
38
SDCHC
E-SE
N
5/8-9
Air #9
ng/m3
1.4
3.6
5.2
N.D.
0.7
2.0
N.D.
1.3
0.9
N.D.
N.D.
N.D.
N.D.
1.6
2.8
N.D.
50
Suburban
E-SE
E-SE
5/8-9
Ait #10
ng/m3
N.D.
1.0
2.2
N.D.
0.4
8.7
N.D.
0.2
0.4
N.D.
N.D.
N.D.
N.D.
3.0
12.7
N.D.
50
Suburban-
Ft , Lauderdale
SE
E
5/10-11/75
ND-Not detectable
All the following pesticides were not detectable: 3 BHC, HCB, Carbofenthion,
p,p'-DDT, o,p'-DDT, mevinphos, methyl bromophos, chlor-
benside, phorate, heptachlpr epoxide, methoxychlor,
ronnel, Thiodan I and II.
-------
Appendix C-/.
Concentrations of pesticides (ng/nT') in air samples collected from several sites in
South Florida 1975-1976
u>
Pesticide
Dichlofenthion
Chlorpyrifos
Diazinon
Malathion
a BHC
Heptachlor
Aldrin
Lindane
Dieldrin
p,pf- DDT
o,p'-DDT
Endrin
Ethyl parathion
Methyl parathion
Methyl bromophos
Phosdrin
a Chlordane
Y Chlordane
Toxaphene
3
m
Air #11
ng/m3
N.D
Interf .
354
24
Interf.
Interf.
Interf.
1.0
Interf.
Interf.
Interf.
Interf.
158
131
N.D.
4,650
Interf.
Interf .
Interf.
50
Location Belle Glade
Wind Direction
Start:
Finish:
Date Collected
Airport
Calm
E
5/19-20/75
Air #12
ng/m3
N.D.
0.5
2.5
6.0
0.1
0.6
N.D.
0.2
0.2
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
3.0
0.4
1.3.
N.D.
51
Miami
Airport
SE
SE
6/10-11
Air #13
ng/m3
0.4
3.0
6.2
N.D.
0.2
1.3
N.D.
0.2
. 0.7
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.6
2.1
N.D.
47
Suburban
E-SE
E-SE
6/10-11
Air #14
ng/m3
N.D.
168
470
170
3,977
7,315
655
4,791
88
73
43
19
86
182
4,130
9
432
2,328
N.D.
52
Formulating
Plant
Indoors
6/11-12
Air #15
ng/ra3
N.D.
1.6
2.9
N.D.
0.3
1.0
N.D.
0.4
0.3
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.3
1.4
N.D.
40
SDCHC
E-SE
E
6/11-12
Air #16
ng/m3
N.D.
0.8
N.D.
2.9
0.3
1.0
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.7
2.2
N.D.
36
SDCHC
Calm
S-SE
7/7-8
Air
ng/
0.
11.
N.
9.
0.
1.
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
0.
2.
N.
51
#17 Air #18
m3 ng/m3
3
5
D.
2
5
1
D.
D.
D.
D.
D.
D.
D.
D.
D.
D.
8
6
D.
Suburban
S-SE
E-SE
7/7-8
N.D.
1.6
N.D.
N.D.
0.5
1.5
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.7
2.0
N.D.
51
Airport
W-SW
SE
7/22-23
Air #19
ng/m3
0.2
1.0
N.D.
1.5
0.9
1.0
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.7
1.7
N.D.
51
Suburban
E-SE
SE
7/15-16
Air #20
ng/m3
N.D.
N.D.
N.D.
N.D.
0.5
0.7
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.2
0.7
N.D.
51
Everglades
S-SE
SW
7/23-24
N.D.-Not detectable
Interf.-Interference
All the following pesticides were not detected: g-BHC, HCB, Trithion,
Ethion, Ronnel, Phorate, Fenthion, Chlorobenside,
Methoxychlor, Thiodan I, Thiodan II and Heptachlor
Epoxide.
-------
Appendix C-3.
Concentrations of pesticides (ng/m ) in air samples collected from several sites in
South Florida 1975-1976
Air #21
Pesticide ng/m3
Dichlof enthion
Chlorpyrifos
Diazinon
Malathion
a BHC
Heptachlor
Y BHC
Ethyl parathion
Methyl parathLon
Bromophos
Mevinphos
Phorate
HCB
a chlordane
Y chlordane
Dieldrin
A BHC
Ronnel
3
m
N.D.
0.7
3.8
1.1
1.0
0.9
1.2
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
1.1
0.5
1.0
N.D.
N.D.
48
Location Suburban
Wind Direction
Start:
Finish:
Date Collected
S-SE
S-SE
8/18-19
Air #22
ng/m3
0.3
0.7
3.6
6.1
0.3
0.6
0.7
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.6
0.7
0.6
N.D.
N.D.
52
Suburban
E-SE
Calm
9/21-22
Air #23
ng/m3
N.D.
0.6
17.6
1.3
1.5
2.1
0.4
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
1.8
2.0
0.5
N.D.
N.D.
52
Suburban
E
NE
10/11-12
Air #24
ng/m3
N.D.
1.5
5.4
N.D.
1.3
2.2
0.8
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
1.2
1.3
0.7
N.D.
N.D.
37
SDCHC
E
S
9/22-23
Air #25
ng/m3
N.D.
1.5
4.2
N.D.
2.2
1.0
1.0
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.9
0.8
0.7
N.D.
N.D.
38
SDCHC
E
NE
10/11-12
Air #26
ng/m3
N.D.
0.6
0.6
1.0
0.9
0.5
0.4
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.2
0.6
0.2
N.D.
N.D.
52.7
Airport
SE
E
10/16-17
Air #27
ng/m3
N.D.
0.5
0.8
N.D.
1.0
2.1
0.7
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.3
0.7
0.2
N.D.
N.D.
37.5
SDCHC
E-SE
Variable
11/25-26
Air #28
ng/m3
N.D.
0.6
0.6
N.D.
0.4
0.8
0.3
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.3
0.8
0.2
N.D.
N.D..
50.3
Suburban
No Data
12/9-10
Air #29
ng/m3
N.D.
65
168
.9
2,301
25,243
3,779
17
Interf .
1,715
Interf.
1
387
597
3,068
24
1,141
2
47.4
Form. Pit.
Indoors
12/12-13
Air #30
ng/m3
N.D.
0.3
0.8
N.D.
N.D.
3.9
0.1
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
0.2
0.9
0.2
N.D.
N.D.
38.6
SDCHC
E
E-NE
12/12-13
N.D.-Not detectable
Interf.-Interference
All the following pesticides were not detected: BBHC, HCB,
Trithion, Ethion, Fenthion, Chlorobenside,
Methoxychlor, Thiodan I, Thiodan II, Toxa-
phene, Heptachlor Epoxide, Endosulfan I,
and Endosulfan II
-------
Appendix C-4. Concentration of pesticides (ng/m^) in air samples collected from several sites in
South Florida 1975-1976
Pesticide
Dichlofenthion
Chlorpyrifos
Diazinon
a BHC
Y BHC
a Chlordane
Y Chlordane
Heptachlor
Dieldrin
m3
Place
j\
j\
Wind - Start
Finish
Date Collected
Air #31
N.D.
22.3
5.9
0.3
0.6
0.9
0.9
1.7
0.3
52.5
Airport
NW
N-rain
1/15-16/76
Air #32
. N.D.
4.5
1.5
0.3
0.6
1.0
1.0
1.4
0.5
46.3
Suburban
NW
N
1/15-16
Air #33 Air #34
N.D.
1.35
0.52
0.20
0.34
0.35
0.98
1.99
0.22
48
Suburban
N
NE
2/10-11
N.D.
0.77
0.63
0.30
0.33
0.41
1.06
3.64
N.D.
49
Airport
E
E
2/10-11
Air #35 Air #36
N.D.
0.51
N.D.
0.10
0.15
0.39
0.41
0.34
0.26
53
Suburban
NE-E
E
3/2-3
N.D.
0.80
N.D.
0.10
0.12
0.30
0.30
0.35
N.D.
52
Airport
E-NE
E
3/2-3
Air #37 Air #38
N.D.
1.00
N.D.
0.20
0.20
0.38
0.43
0.66
0.28
52 '
Suburban
E-NE
E
3/5-6
N.D.
N.D.
N.D.
0.13
0.16
0.16
0.19
0.64
0.30
36
Air #39 Air #40
N.D.
1.40
N.D.
0.21
0.22
0.42
0.50
0.72
N.D.
49
So. Dade Suburban
Comm.
E-SE
SE
3/5-6
Hlth
SE
E
3/15-16
N.D.
N.D.
N.D.
0.17
0.15
0.15
0.19
0.67
0.27
37
So. Dade
Comin.
E-SE
E
3/16-17
N.D. = Not detectable
All the following pesticides were not detectable: Dichlofenthion,
malathion, aldrin, lindane, p.p'-DDT, o,p'-DDT, aldrin,
ethyl parathion, methyl parathion, A BHC, HCB, ronnel,
trithion, ethion, phorate, bromophos, fenthion, methoxy-
chlor, heptachlor epoxide, Thiodan I and Thiodan II.
-------
Alkyl phosphates
BHC
Bromophos
Carbaryl
Chlorpyrifos (Dursban)
cholinesterase
DEF
Diazinon
Dichlofenthion (VC-13)
Dlchlorvos (DDVP)
Ditnethoate (Cygon)
Ethyl parathion
HCB
Heptachlor
Heptachlor Epoxide
Lindane
LD50
Malathion
GLOSSARY
degradation products; urinary metabolites .
1,2,3,4,5,6 hexachlorocyclohexane
(mixtures of isomers)
0-(4-Bromo~2,5-dichlorophenyl)
0,0-dimethyl phosphorothioate
1-naphthyl N-methylcarbamate
0,0-diethyl 0-(3,5,6 trichloro-2-pryidyl)
phosphorothioate
An esterase present in all body tissues
which hydrolyzes acetylcholine into
choline and acetic acid
s,s,s-tributyl phosphorothioate
0,0-Diethyl 0-(2-isopropyl-6-methyl-4-
pyrimidinyl) phosphorothioate
0,0-Diethyl-O-(2,4-dichlorophenyl)
phosphorothioate
2,2-Dichlorovinyl dimethyl phosphate
0,0-Diinethyl-S-(N-methylcarbamoylinethyl)
phosphorothioate
0,0-Diethyl 0-p-nitrophenyl phosphorothioate
Hexachlorobenzene (fungicide)
l,4,5,6,7,8,8-Heptachloro-3a,4,7,7a-
tetrahydro-4,7-raethanoindene
1,4,5,6,7,8,8-Heptachloro-6,7-epoxy-3a,
4,7,7a-tetrahydro-4,7-methanoindene
Gamma isomer of benzene hexaehloride
(1,2,3,4,5,6-hexachlorocyclohexane)
of 99+% purity
in toxicity studies it is the dosage
required to kill 50% of the test animals
when given a single dosage by mouth or
skin contact. The dose is expressed by
the weight of the chemical per unit of
body weight.
0,0-Dimethyl S-[l,2-bis(ethoxy-carbonyl)
ethyl] phosphorodithioate
66
-------
Methyl parathion
Mevinphos (Phosdrin)
M.R.I.
Naled (Dibrom)
Not Detected
PCP
PNP
p,p'-DDT
p,p'-DDE
o,p'-DDT
o,p'-DDE
2,4-DCP
2,4-D esters
2,4,5-T esters
2,3,4,6-TTCP
0,0-Dimethyl o-p-nitrophenyl phosphorothioate
0,0-Dimethyl 1-carbomethoxy-l propen-2-yl
phosphate
Air sampling unit built by Midwest Research
Institute and used in air monitoring studies
by E.P.A.
1,2-Dibromo-2,2-dichloro-ethyl dimethyl
phosphate
Below the limits of detectability in the
gas chromatograph
2,3,4,5,6 Pentachlorophenol
paranitrophenol - a urinary metabolite of
parathion, EPN, methyl parathion and chlorthion
1,1-Bis-(p-chlorophenyl)-2,2,2-trychloroethane
2,2-Bis-(p-chlorophenyl) 1,1-dichloroethylene
1-(0-chlorophenyl)-1-(p-chlorophenyl) 2,2,2-
trichloroethane
1-(o-chlorophenyl)-1-(p-chlorophenyl)-2,2-
dichloroethylene
2,4-Dichlorophenol
2,4-dichlorophenoxy acetic acid
2,4,5-trichlorophenoxy acetic acid
2,3,4,6 tetrachlorophenol
67
-------
TECHNICAL REPORT DATA
(Please read Instructions on the reverse before completing)
1. REPORT NO.
EPA-600/1-77-019
3. RECIPIENT'S ACCESSION-NO.
4. TITLE AND SUBTITLE
Occupational and Environmental Pesticide Study in
South Florida
5. REPORT DATE
April 1977
6. PERFORMING ORGANIZATION CODE
7. AUTHOR(S)
John E. Davies
8. PERFORMING ORGANIZATION REPORT NO
9. PERFORMING ORGANIZATION NAME AND ADDRESS
University of Miami School of Medicine
1600 N.W. 10th Ave.
Miami, FL 33152
10. PROGRAM ELEMENT NO.
1EA615
11. CONTRACT/GRANT NO.
68-02-1760
12. SPONSORING AGENCY NAME AND ADDRESS
Health Effects Research Laboratory - RTF, NC
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park. N.C. 27711
13. TYPE OF REPORT AND PERIOD COVERED
14. SPONSORING AGENCY CODE
EPA/600/11
15. SUPPLEMENTARY NOTES
16. ABSTRACT
Studies of the urinary pesticide metabolites demonstrated that alkyl phosphates
were highly sensitive indices of recent exposures to DMP and DEP organophosphate
pesticides. In contrast, urinary phenolic metabolites when available provided sensitive
Urinary metabolites furthered laboratory confirmation of poisonings and facilitated the
recognition of subtle differences in organophosphate exposures, properties which lend
themselves to use in human monitoring and epidemiologic studies of the occupationally
exposed. Urinary alkyl phosphate excretions permitted the recognition of worker pro-
tection from residues in the field acquired by wearing fluorocarbon treated clothing.
Being group specific rather than pesticide specific, urinary alkyl phosphates were
unsatisfactory surveillance instruments when cholinesterase depression or illness was
the disease end point of concern and when pesticide exposures were mixed. Important
sources of pesticide exposure in a formulating plant included high concentrations in
the air and contaminated workers' clothing. Bromophos, a fat soluble organophosphate,
was identified in fat for the first time in three formulators, and modification of the
analytical laboratory procedures for pesticides in air and in fat increased the number
of pesticides identified in air and the recognition of the less polar organophosphates
in fat.
17.
KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS
b.lDENTIFIERS/OPEN ENDED TERMS C. COSATI Field/Croup
Pesticides
Metabolism
Urine
Organic phosphates
Epidemiology
Diagnostic agents
06 A
06 T
18. DISTRIBUTION STATEMENT
RELEASE TO PUBLIC
19. SECURITY CLASS (ThisReport)
UNCLASSIFIED
21. NO. OF PAGES
83
20. SECURITY CLASS (Thispage)
22. PRICE
EPA Form 3220-1 (9-73)
68
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