Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue.

Organochlorine Pesticides and Polychlorinated Biphenyls in Human Adipose Tissue* Frederick W. Kutz**, Patricia H. Wood***, and David P. Bottimore*** Contents I. II. III. IV. V.

Introduction .................................................. Aldrin/Dieldrin/Endrin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . BHC ......................................................... DDT and Related Compounds. . ... .. . .. . ... .... . . ........... . . . Heptachlor/Heptachlor Epoxide, Chlordane/Oxychlordane, trans-Nonachlor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . VI. HCB . . . . . . . . . .. .. . . . . . ... . .. . . .. . .... . ....... . .. . . . . . . . ... . . . VII. Mirex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . VIII. PCBs ........................................................ IX. Toxaphene ................................................... Summary .......................................................... Explanation of Names and Abbreviations Frequently Shown on the Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

1 7 14 28 42 51 55 61 65 71

73 74 74

I. Introduction The U.S. Environmental Protection Agency (U.S. EPA) has estimated that approximately 750,000 chemicals are now in use in hpmes, industry, and agriculture. This does not include pesticides, pharmaceuticals, and food additives, nor the estimated 1,500 different ingredients used in pesticides (Geyer et al. 1986). * Although funded by the U.S. Environmental Protection Agency through Contract Nos. 68-02-4254 and 68-D9-0166 to Versar Inc., this contribution has not been subjected to Agency review and therefore does not necessarily reflect the views of the Agency and no official endorsement should be inferred. **Office of Modeling, Monitoring Systems and Quality Assurance, Office of Research and Development, U.S. Environmental Protection Agency, 401 M Street S.W., Washington, DC 20460. ***Versar Inc., Environmental Operations, 6850 Versar Center, Springfield, VA 22151.

© 1991 by Springer-Verlag New York Inc. Reviews of Environmental Contamination and Toxicology. Vol. 120.

2

F.W. Kutz, P.H. Wood, and D.P. Bottimore

The release of a chemical into the environment suggests the need for knowledge of its geographical transport, its chemical transformation, its possible impact on target organisms, and its fate as well as the identity and fate of its metabolites. Exposure of humans to chemicals and their ultimate effects can be represented by the following: Source -+ Environmental -+ Environmental -+ Exposure/ Pathway Conditions Dose -+

Dose -+ Effects Delivered

Exposure to chemicals in the environment occurs through contamination of food, air, and/or water. Exposure can be either direct or indirect, or may involve multiple routes. In many cases it is difficult to determine exactly the route(s) of exposure. Direct exposure may involve inhalation or dermal contact with a point source and generally occurs in the course of manufacture, use, transportation, or disposal. Indirect exposure occurs through contact with a chemical after it has been distributed in one or more environmental media, and has been subjected to natural transformation and accumulation processes. In order to identify exposure pathways, information is needed about the chemical's identity, its chemical and physical properties, its environmental fate and transport, and its sources. After the principal pathways of exposure have been identified, monitoring data are used to estimate releases and environmental concentrations. These releases and environmental concentrations are used to estimate the amount of chemical to which individuals may be exposed. Once a chemical enters the body, it may undergo extensive biotransformation. Some chemicals are rapidly metabolized and excreted from the body in the urine and/or feces; others are slowly metabolized and undergo extensive storage in tissues, finally passing through the body virtually intact. Along with exposure studies, therefore, studies of tissue storage of xenobiotics are relevant to human health. For instance, most highly lipophilic chemicals such as the halogenated organic compounds are slowly biotransformed, and tend to concentrate in the body fat tissue (e.g., adipose tissue). The halogenated organic compounds reviewed in this contribution include the organochlorine insecticides aldrin, dieldrin, endrin, chlordane, oxychlordane, heptachlor, heptachlor epoxide, trans-nonachlor, hexachlorocyclohexane, dichlorodiphenyltrichloroethane (DDn and related compounds, toxaphene, and mirex, in addition to hexachlorobenzene and polychlorinated biphenyls (PCBs) (Chemical names are provided within the specific chapters). Monitoring studies have shown that these organic compounds are stored in the adipose tissue of humans and animals.

Residues in Human Adipose

3

As a group, all these complex halogenated organic compounds are highly persistent in the environment because of their stable chlorinated ring structure. This persistence leads to potential incorporation into the food chain and subsequent uptake by humans. Because these compounds are extremely lipophilic and are metabolized very slowly, chronic exposure, mainly through the food chain, has led to accumulation of both the parent compounds, and their metabolites in human adipose tissue. For many years, residues of halogenated organic compounds have been detected in the human adipose tissue of individuals in a number of countries, including those living in Europe, Asia, and Africa, as well as in the North America. The levels detected have been used as an index of the level of exposure of the general population to these compounds over time. Over the past two decades, most countries have observed a steady decline of chlorinated hydrocarbon storage and exposure, reflecting a reduction in the use of these compounds, restrictions on or banning of their use, and a corresponding decrease in their environmental levels. Studies have also been conducted on the levels of organochlorine compounds found in adipose tissues as they relate to such demographic factors as age, sex, race, particular physiological states, and living and working conditions. To determine the trends of concentration levels in the adipose tissue of the general population, monitoring studies have been conducted in the United States and some foreign countries. Many of these efforts are described briefly below. The National Human Monitoring Program (NHMP) was established in the United States in 1967 to monitor the levels and prevalence of chemicals in humans and the environment. The program was initiated by the U.S. Public Health Service, but was transferred to the U.S. EPA in 1970. The National Human Adipose Tissue Survey (NHATS) is a major component of NHMP. Its purpose is to detect and quantify the prevalence of selected toxic compounds in the general population. Specimens are collected from autopsied cadavers and surgical patients according to a statistical multi-stage sampling design. The NHA TS is designed to select a representative national sample of adipose tissue specimens every year. The specimens are supplied to EPA by selected pathologists and medical examiners, along with associated demographic, occupational, and medical information. The presence of a substance in adipose tissue is an indication of its presence in the environment, usually food, water and/or air. By selecting and chemically analyzing the tissues of a representative sample of individuals, information is then available for determining existing residue levels in the U.S. population as a whole. Moreover, this survey also provides information to identify various subpopulations and to assess trends in levels of the chemical substances (U.S. EPA 1986a). The adipose tissue specimens

4

F.W. Kutz, P.R. Wood, and D.P. Bottimore

are collected annually and are chemically analyzed for twenty chlorinated hydrocarbon compounds, including PCBs. The specific objectives of the adipose tissue survey are: (1) to assess the prevalence of these substances in the adipose tissue of the general U.S. population, (2) to measure time trends of these concentrations, (3) to assess the effects of regulatory actions on the levels of concentration, and (4) to establish baseline levels for the selected compounds in adipose tissue (U.S. EPA 1985b). The chemical residue analysis of NHA TS samples involves a threshold value below which a sample cannot be accurately quantified; this threshold is called the level of quantification (LOQ). Another threshold level below the LOQ is called the level of detection (LOD). At this threshold level, the presence of a compound in the sample cannot be ascertained as detected. Values below the LOD are reported as not detected; values measured between the LOD and LOQ are reported as trace values. NHATS data values are sometimes reported as "lipid adjusted." These data were obtained by dividing the measured residue concentration in the total sample by the decimal fraction of the sample that consists of ether-extractable lipid. The Federal Republic of Germany established an Environmental Specimen Bank for Human Tissue at the University of Meunster in 1977. One task of this pilot specimen bank is to maintain a continuous surveillance for possible changes in the concentration patterns and trends of xenobiotics in human samples (real-time monitoring) (Bertram et al. 1986). In Germany, organochlorine pesticides have been analyzed in the adipose tissue and blood of living people, using real-time monitoring, as well as in autopsy material (Bertram et al. 1986). Czechoslovakia has a long tradition of monitoring environmental organochlorine pesticide contamination. Monitoring for residues of organochlorine chemicals in adipose tissues from the general population began as a result of the country's widespread use of DDT (Hruba et aL t 984). Monitoring was originally conducted in 1960-62, was initiated a second time in 1971-74, and was performed again in 1980-81. Rumania has also conducted several surveys to determine the concentration of organochlorine pesticides in the adipose tissue of the general population. The surveys, conducted in 1965-66, 1967-68, and 1971-72, were to determine specifically the concentration of total DDT and total BHC in the general population. In the last survey (1971-72), an increase (from 4.34 ppm in 1965-66 to 5.12 ppm) in the level of BHC concentrations and a decrease (from 17.34 ppm in 1965-66 to 3.33 ppm) in the level of DDT concentrations were noted. These trends were believed to result from a decreased DDT use, an increase in use of BHC, and a greater emphasis on proper labeling and use of agricultural products (Aizicovici et al. 1974). In Canada, Ontario banned the use of aldrin, dieldrin, and heptachlor in 1969 and curtailed the general use of DDT in early 1970. The use of DDT


5

was subsequently canceled in late 1970. Canada then conducted a monitoring program to determine the level of organochlorines in adipose tissue and to ascertain whether restrictions on use affected organochlorine contents of these tissues. PCBs and HCB were also measured (Holdrinet et al. 1977). Many other published studies also reported the levels of halogenated organic compounds in human adipose tissue. This contribution will summarize the tissue level data for the specified organochlorine chemicals from these studies, and will briefly present relevant physicochemical, toxicological, monitoring, exposure, and regulatory data. According to Kutz (1983), monitoring data are critical factors in assessing exposure and evaluating risks. Studies of laboratory animals determine the actual or potentially adverse biological activity (toxicity) of a chemical, while monitoring data are used to assess the exposure of selected human and environmental components to the chemical. Monitoring studies also contribute substantial information about the intermediate and final environmental fate of pesticides and other toxic chemicals. The development of information related to the adverse health effects of pesticides and other toxic chemicals on human beings is a primary objective of monitoring programs, the media and chemicals selected must be those that contribute efficiently to understanding these effects. Thus, monitoring programs are designed to develop scientific information that describes: (1) the direct and indirect pathways of human exposure, (2) the health, economic, and ecological impacts of the exposure, and (3) the processes of mobility, metabolism, bioaccumulation, and degradation that affect pesticide transport in the environment. Monitoring is a general term used to describe a variety of activities. Basically, chemical monitoring is an investigative activity that periodically samples selected environmental or human materials and then analyzes these specimens for evidence of chemical residues indicative of potential human, animal, or plant exposure. These activities are aimed at developing statistical measures of residues in particular human or environmental matrices. Some chemical molecules are transformed by abiotic processes such as hydrolysis or photodecomposition or by microbially mediated degradation to produce other compounds that are identifiable as degradation products of the original chemicals. Monitoring activities can be viewed as containing four basic elements: (1) survey design, (2) specimen collection and processing, (3) chemical analysis, and (4) data analysis and interpretation. These elements may also be used to evaluate the validity of monitoring studies (Kutz 1983). Most monitoring studies are predicated on a statistical survey design developed to fulfill certain objectives or answer specific questions, such as geographic variation and temporal trends. The design ultimately determines the interpretation of the results, as well as the accuracy and precision of the study. In general, the design describes the objectives of the study and

6


prescribes the method for selecting the sample parameters. Included in the design description is a clear explanation of the biases that were considered during design development and a quality assurance program. During specimen collection and processing, selected matrices are collected and handled in accordance with the survey specifications. It is important to be able to verify that the specimens were collected as specified by the design. If sampling procedures are altered, then specific exceptions must be noted. Most survey designs list appropriate measures that should be taken if a particular sampling parameter is unavailable. The chemical analysis of specimens is the phase in which the actual determination of the residue(s) of interest is made. It usually consists of two steps: (1) extraction and (2) instrumental analysis. During the extraction step, the residue of interest is separated from the physical sample matrix, and from other chemical substances that may interfere with its precise identification and measurement. These extraction steps are usually based on the physical and/or chemical properties of the residue in question and the matrix in which it is contained. The instrumental analysis must frequently involve the use of sophisticated instrumentation, such as gas chromatography/mass spectroscopy, to measure the exact amount of residue present in the extraction sample. Such instrumentation is generally capable of separating related chemicals as well as producing a response in a detection system that is in some way proportional to concentration. An important feature of the instrumental analysis is the exact detection system used to identify, quantitate, and confirm the presence of the residue of interest. Under most conditions, the more a particular detection system has been used, the more reliable the data become. It is also important to note that the correct identity of residues found in monitoring studies needs to be sufficiently established to permit the use of the data in forensic circumstances. Special monitoring studies usually involve fewer samples and hence generate fewer data. Often, the amount of data from special studies restricts the statistical interpretation, thus placing some limits on extrapolations and projections. The statistical interpretation of monitoring data requires special attention. Because most monitoring data are not distributed according to a normal distribution curve, parametric statistical tests and procedures are not always appropriate. Since many statistical tests and manipulations assume normality, they cannot be applied directly to all monitoring data without certain transformations. However, nonparametric or distribution-independent statistical methods are available to use in these situations. These statistical methods make use of some unique statistics, such as the geometric mean, median, percentile distribution, and other applications for treating nonparametric distributions.


7

The final report of a monitoring study generally includes adequate consideration of the data developed via the quality assurance program. This information provides the basis for weighing the validity of the study. In addition, data from studies that do not conform to these standards should not be ignored. Although such data may not be useful quantitatively, in some cases, such data can provide additional evidence of human or environmental exposure (Kutz 1983). II. Aldrin/Dieldrin/Endrin Aldrin is the common name approved by the International Standards Organization (ISO) for an insecticide containing not less than 95% (w/w) of the chemical (1,2,3,4,10,1 0-hexachloro-1,4,4a,5,8,8a-hexahydro-l ,4-endo-exo-, 8,dimethanonapthalene) HHDN (Brooks 1974). Technical grade aldrin contains not less than 90% of aldrin. Dieldrin is the common name approved by ISO (except in Canada, Denmark, and the USSR) for an insecticide containing not less than 85% weight of (1,2,3,4,10,1 0-hexachloro-6, 7-epoxy-l ,4,4a,5,6, 7,8,8a-octahydro1,4-endo-exo-8-dimethanonapthalene) HEOD (Hayes 1982). In most countries, the common name dieldrin stands for the technical product that contains not less than 95% (w/w) of dieldrin as defined above. In Canada and the USSR, dieldrin is referred to as the pure compound, and in Great Britain it is known as HEOD. Endrin (1,2,3,4, to, 10-hexachloro-6, 7-epoxy-1,4,4a,5,6, 7,8,8a-octahydro1,4-endo-5,8-dimethanonapthalene) is a stereoisomer of dieldrin. Endrin is the common name approved by ISO except in India and South Africa where it is called mendrin. Technical endrin contains not less than 92% by weight of endrin (Hayes 1982). Aldrin, dieldrin, and endrin are all cyclodiene chemicals and, like other organochlorine chemicals, they are lipophilic. Unlike aldrin, dieldrin and endrin have a low vapor pressure and therefore are very persistent in the environment. Each chemical has been identified in such environmental media as surface waters, drinking water, rainwater, soil, air, plants, and animals (WHO 1979a; Brooks 1974). Many studies have shown that aldrin is readily expoxidized to dieldrin by mammals, soil microorganisms, plants, and insects (Matsumura 1975; WHO 1979a). Therefore, aldrin is found less often and in smaller quantities than dieldrin. Endrin is the epoxidized metabolite of isodrin, a rarely encountered cyclodiene. Aldrin, a soil insecticide, is the major source of dieldrin in the environment. Both compounds are rapidly adsorbed onto the soil. Aldrin, dieldrin, and endrin can enter the air through volatilization from treated crops and soil

8


during application. Dieldrin is also found in soil and water surfaces as a result of washout and dry deposition (WHO 1989). Analyses have shown that contamination of the environment with dieldrin and aldrin is widespread. These occurrences have been found principally as dieldrin in the air, terrestrial ecosystems, the aquatic environment and organisms, food, and even in human tissues and human milk. Dieldrin has also been found in dairy and meat products, fish, oils, fats, and certain vegetables (WHO 1979a). Aldrin and dieldrin are organochlorine insecticides that have been manufactured commercially since 1950 and were widely used in agriculture throughout the world up to the early 1970s. Both compounds were registered for use in the United States in 1949. By February 1973, dieldrin was approved in the U.S. for use on approximately 46 agricultural crops. Both compounds act as stomach and contact poisons for insects and have been used as insecticides in agriculture in the treatment of seed and for the control of soil pests. Insects controlled by these insecticides include termites, crickets, grasshoppers, wood borers, beetles, and textile pests (moths that feed on woolen clothing and carpets) (U.S. EPA 1987a). Dieldrin is also used for public health purposes for the control of the tsetse fly and other vectors of debilitating tropical diseases in developing countries. Since aldrin is more volatile than most organochlorines, it is less persistent than the epoxides. It was used in foliage applications where immediate destruction and a short residual effect were required (Brooks 1974). Its high vapor pressure produces a slight fumigant effect, which reaches soil insects whose habitat is inaccessible to other compounds. Dieldrin is more valuable for surface treatments because of its lower volatility; such use controls insects living or feeding at soil level. Aldrin was used to control pests on bananas, orchard fruit, potatoes, sugar beets, sugarcane, tobacco, and corn, and also recommended for use on figs and dates, ornamentals, yams, and soybeans (Brooks 1974). Endrin could also be applied to any of the above plants, especially those plants where dieldrin use was favored. Its main use, however, was for foliage applications. Endrin was used to protect tropical crops such as maize, rice, sugarcane, tobacco, coffee, and cocoa; grasses and trees; forage crops such as alfalfa; and some orchard crops. Perhaps its most effective use was against cotton pests. Domestically, most aldrin and dieldrin use was banned in 1975. Today, these compounds are no longer produced or imported into the U.S. In 1985, all uses were banned except for subsurfaces oil treatment for termites, dipping of nonfood roots and tops, and mothproofing undertaken during the manufacturing process (Dynamac 1987a). Currently, all uses of aldrin and dieldrin in the U.S. have been voluntarily canceled or suspended (Polpyk 1989). The only remaining registered use for endrin is as an avicide, particularly for


9

establishments such as airports where birds can be sucked into airplane propellers and jet engines. (Personal communication with George Larocco, U.S. EPA, Office of Pesticide Programs.) Since the 1970s, use of these two compounds has been restricted or banned in some foreign countries for agricultural purposes (WHO 1989). However, these compounds are still being used in other countries for termite control. Aldrin is prohibited in a number of countries, including Argentina, Brazil, Canada, Chile, Ecuador. Finland, the German Democratic Republic, Hungary, Japan, Singapore, Sweden, Switzerland, and the USSR. The European Community Legislation prohibits the marketing of phytopharmaceutical products containing aldrin or dieldrin. In Finland, aldrin and dieldrin are prohibited for agricultural use, but both the chemicals can be employed as termiticides in a glue mixture used in export plywood. Dieldrin is prohibited for use in agriculture in many countries, including Brazil, Ecuador, Finland, the German Democratic Republic, Singapore, Sweden, Yugoslavia, and the USSR. Use is prohibited, with some exceptions, in Argentina, Canada, Chile, the Federal Republic of Germany, and Hungary. Industrial uses are prohibited in Switzerland, and its manufacture and use are controlled by the government in Japan. Its use is restricted in India, Mauritius, Togo, and the United Kingdom. Dieldrin, aldrin, and endrin are toxic to man and other mammals. Although there is limited evidence of carcinogenicity in experimental animals, none of these chemicals can be classified as carcinogenic to humans. All available studies show that these chemicals are not related to cancer incidences in humans (WHO 1989). Mammalian metabolism of these chemicals is confined mainly to the liver. Aldrin is readily converted to dieldrin; therefore, exposure to aldrin signifies exposure to dieldrin as well. Aldrin is rarely found in blood or other tissues except in cases involving acute ingestion of large doses. Dieldrin is slowly degraded to hydrophilic metabolites; these metabolites are then excreted in the bile and the urine. Endrin is generally more toxic than dieldrin; there is no explanation for this difference at present (U.S. EPA 1980c). Endrin is eliminated very rapidly from mammalian tissues. It shows little tendency to undergo storage and is only detected in human tissue immediately after an acute overexposure (Brooks 1974). The absence of measurable levels of endrin in human subcutaneous fat or blood, even in areas where it has been used extensively, such as in India and the lower Mississippi, leads to the conclusion that despite its relatively high acute toxicity, endrin is nonpersistent in man (Brooks 1974). Presently, the most probable source of human exposure to aldrin, dieldrin, or endrin will be as a result of their presence in improperly managed waste sites (U.S. EPA 1987a). Persons can absorb aldrin, dieldrin, and endrin

52 54

1972 6

Frequency (percent) ND 0.193

Average Concentration (ppm) GLC-ECD

Analytical Method

Garcia Fernandez (1971) Syrowatka et al. (1978)

Reference

1975

1969-70 1971-72 1972 1973-74 1976 1979-81 1980-81 Oct 81-Feb 82

Argentina Belgium

Belgium Canada Canada Canada Canada Canada Canada Canada, Kingston Canada, Ottawa Costa Rica

Geographical Area

51 29 37 282 168 129 99 91 84 30

52 60

Date of Sample No. of Collection Samples

100 88 95 17

100

Frequency (percent)

0.12 0.046 0.17 0.13 0.069 0.09 0.049 0.036 0.043 0.16

0.07 0.26

Average Concentration (ppm)

GC-MS GC-ECD GC-ECD GLC-ECD

GC-MS

GLC-ECD

GC-ECD

Analytical Method

Garcia Fernandez (1971) Dejonckheere et al. (1978) Van Haver et al. (1978) Mes et al. (1985) Holdrinet et al. (1977) Holdrinet et al. (1977) Mes et al. (1977) Holdrinet et al. (1977) Mes et al. (1982) Williams et al. (1984) Williams et al. (1984) Barquero and Constenla (1986)

Reference

Table 2. Levels of dieldrin detected in human adipose tissue in the general population of various countries

Argentina Poland, Warsaw

Geographical Area

No. of Samples

Date of Sample Collection

Table 1. Levels of aldrin detected in human adipose tissue in the general population of Argentina and Poland

a

o

S·

o

:::

t:I:I

~

O

P-

::s

Pl

~

o

~

~

'"C

.N'

~

~

~

'Tl

o

-

1975

1969 1973 1970-71

1963-4 1963-4 1965-7 1965-7 1969-71 1976-7 1965-7

Mexico, Mexico City

Netherlands New Zealand Pakistan

United Kingdom (males) United Kingdom (females) United Kingdom (males) United Kingdom (females) United Kingdom United Kingdom USA, Dade Co., FL USA, Dade Co., FL

USA, Hawaii USA, Hawaii

1974-75 1979 1975

1973-74 1971

1974-76

282 48

Spr 82-Spr 83

30

43 23 157 91 201 236 146 42

51 60

9

28 21 241 59 32 19

170

11

82

1972-73

Italy Japan (females) Japan Japan Japan, Osaka Mexico, Torreon

Denmark France W. Germany W. Germany (children) Holland Iran

96

89

58

92 100

85

0.027 0.040

0.27 0.23 0.23 0.18 0.16 0.11 0.22 0.215

0.27 0.21 0.047

0.18

0.29" 0.33 0.13 0.09 0.14 0.06

0.13" 0.40 0.14 0.03 b 0.17" 0.049 Kraul and Karlog (1976) Fournier et a1. (1972) Schulte (1975) HPLC Niessen et a1. (1984) Nonhydro de Vlieger et a1. (1968) GC-ECD Hashemy-Tonkabony and Soleimani-Amiri (1978) GC-ECD Leoni et a1. (1978) GLC Doguchi et a1. (1971) GC-ECD Curley et a1. (1973) GLC Yoshimura et a1. (1979) GC Yoshimura et a1. (1981) GLC-ECD Albert and Mendez (1980) GLC-ECD Albert and Mendez (1980) Wit (1971) GLC-ECD Solly and Shanks (1974) Colorimetric/TLC Mughal and Rahman (1973) GLC Abbott et al. (1972) GLC Abbott et a1. (1972) GLC Abbott et a1. (1972) GLC Abbott et al. (1972) GLC Abbott et a1. (1972) GLC Abbott et a1. (1981) GLC-ECD Edmundson et a1. (1968) GC-ECD Fiserova-Bergerova et a1. (1967) GC-ECD Casarett et a1. (1968) Morgan and Roan (1970)

GLC-ECD

s.:

~ C1>

C1>

Of>

0

Po -6.

;I>

1:3

~

!:=

= 8

S·

Of>

C1>

!:=

Of>

Idaho Miami, FL Tucson, AR Texas Texas

b

a

Geometric mean. Median.

USA, Monroe, LA USA, Monroe, LA USA, Dade Co., FL (females) USA, Monroe, LA USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) Zaire

USA, USA, USA, USA, USA,

Geographical Area

Table 2. (Continued)

1984 1970 1971 1972 1973 1974 1975 1976 1977 1978 1979 1981 1983 1983

10 10 1412 1616 1916 1092 898 779 681 786 816 796 384 407

22 8

70 221 35

1968-9 1969-72 1987-88

1977 1980

200

No. of Samples

1970


100 100 96.46 99.20 98.28 98.99 99.00 95.5 93.7 95.5 95.7 94.8 88.5 95.3

100

98

Frequency (percent)

0.15 0.10 0.18 a 0.21a 0.18" 0.18" 0.1s" 0.12" 0.09" 0.09" 0.09" 0.08" 0.05" 0.06" 0.26

0.15 0.15

0.2 0.215 0.140 0.35 0.036'


Barquet et a1. (1981) Holt et a1. (1986) Kutz et a1. (1976) Kutz et a1. (1976) Kutz et a1. (1976) Kutz et a1. (1977) Kutz et a1. (1977) US. EPA (unpub.) US. EPA (unpub.) US. EPA (unpub.) U.S. EPA (unpub.) US. EPA (unpub.) US. EPA (unpub.) US. EPA (unpub.) Okond Ahoka et a1.

GC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-MS

(1984)

Greer et a1. (1967) Holt et a1. (1986)

(1988)

Wyllie et a1. (1972) Morgan and Roan (1970) Morgan and Roan (1970) Burns (1974) Adeshina and Todd

Reference

GLC-ECD GLC-ECD

GLC-ECD GC

Analytical Method

(1)

'"1

0

0

t:I:l

-3'

t:I ~

Q.

::l

~

F-

~ 0 0

F 'tI ;t

~

s::

~

'Tl

N

..-


13

through inhalation or by absorption through the skin, especially in areas where the compounds are used to treat crops. Since the ban on the use of aldrin and dieldrin, the potential for exposure has diminished considerably. The highest previous non-occupational exposure was probably experienced by occupants of residences treated with aldrin for termite control (U.S. EPA 1987a). The most common source of general population exposure to aldrin and dieldrin is believed to have been contaminated food products. In the past, human exposure occurred because of eating foods grown in contaminated soil. Other contaminated food were fish, poultry, and beef which were previously exposed to these insecticides. Exposure could also result from drinking milk or water containing these compounds, although water concentrations have been extremely low. Contaminated food products are believed :0 have been the primary source of dieldrin residues found in the human adipose tissues of the general population. The National Human Adipose Tissue Survey (NHA TS) for fiscal years 1970-1983 tested for aldrin. Although that compound was essentially not detected, its metabolite, dieldrin, was discovered. Global surveys have shown that mean values in human adipose tissue in the U.S. and some foreign countries range from 0.04 to 0.35 ppm for dieldrin. Available literature from this survey indicates that aldrin has been detected only in the human adipose tissues of the general population of two countries, Poland and Argentina. Also, the literature does not show that levels of endrin have been detected in human adipose tissues. Since the use of these compounds has been banned or restricted, there has been a steady but slow decrease in levels of aldrin and dieldrin in some food commodities. Therefore, since the major exposure to the general population was through the food chain, some decrease in the

1970

1971

1972

1973

1974

1975

1976

1977

1978

1979

1981

Fig. 1. National Human Adipose Tissue Survey (lipid adjusted): dieldrin.

1983

14


levels in human tissues, including adipose, has been shown since the early 1970s (see Tables 1 and 2, and Fig. 1).

III. BHC Benzene hexachloride (BHC), is known chemically as (1,2,3,4,5,6-hexachlorocyclohexane). Although BHC is the most widely used common name for this chemical, particularly in the U.S., other common names include 666 (Denmark), hexaklor (Sweden), hexachloran (USSR), and HCH (most countries in Europe). The name BHC is a misnomer because this chemical is a saturated chlorinated hydrocarbon and is thus not aromatic. BHC is a broad-spectrum insecticide of the group of cyclic chlorinated hydrocarbons. Technical grade BHC consists of a mixture of five configurational isomers of alpha (60 to 70%), beta (5 to 12%), gamma (10 to 15%), delta (6 to 10%), and epsilon (3 to 4%) (Metcalf 1981). The gamma isomer, commonly referred to as lindane, is the most prevalent and has the highest acute mammalian and insecticidal toxicity. In a strict historical sense, BHC could be the oldest of the organochlorine insecticides. Its pure chemical origin can be traced back to 1825, when it was first synthesized by Michael Faraday. Its insecticidal properties were first discovered independently by French and English chemists in the early 1940s. These coincidental discoveries were the result of the need to replace the loss of overseas sources of agricultural insecticides during World War II. Also during this period, the insecticidal activity of BHC was shown to be due almost entirely to the presence of the gamma isomer. The only known usage of BHC was as an insecticide. It was registered for use in the U.S. on a wide variety of fruits, vegetables, and field crops, as well as for use on uncultivated land intended for general outdoor activities and on breeding stock. It proved effective in the control of all major cotton pests with the exception of the bollworm and spider mites. A dip or spray containing the gamma isomer controlled lice on cattle, sheep, and goats, killing all forms (including the egg) of the pests. BHC was also used in the control of malaria and other vector borne diseases. By 1978, all products containing BHC registered in the U.S. were eliminated. In some instances, the products were discontinued voluntarily; in others, registrants reformulated their products to incorporate lindane (at. least 99% pure gamma isomer) rather than BHC (U.S. EPA 1985a). Relative to other insecticides, BHC, including lindane, was used less extensively in the U.S. and in western Europe than in other countries. Also, the proportion ofBHC used as a crude mixture of isomers rather than as lindane was greater in other countries (Hayes 1982). Countries that have reported the use ofBHC include Australia (bananas, corn, leafy vegetables, potatoes); Guatemala (coffee, corn); India (wheat, rice); the United Kingdom (apples, leafy


15

vegetables) (U.S. FDA 1981); and Japan (WHO 1979a). According to WHO, the use ofBHC and lindane was discontinued in Japan in 1971 (WHO 1979a). Lindane or gamma BHC was registered in the U.S. for the following uses: (1) foliar or soil applications on fruit and vegetable crops and on lawns and turf; (2) seed treatments on a variety of field crops; (3) dips and sprays to control pests on livestock and pets; and (4) agricultural premise treatment. Lindane is of importance in topical treatments for the control of human ectoparasites. It was effective against mosquitoes, and flies and livestock ectoparasite that had become resistant to DDT. Lindane was also used for the control of household and garden insects. However, the use of lindanecontaining products in vaporizers and smoke fumigation devices was discontinued in the u.s. Lindane-containing products are now used only under Special Local Needs Registrations (U.S. EPA 1985a). Lindane is an important organochlorine pesticide used extensively for agricultural and public health purposes in India, and other developing countries. Lindane appears to be used on a variety of crops throughout the world: Argentina, Barbados, Germany, Canada, Sudan, Nigeria, and France, to name a few (U.S. FDA 1981). BHC and lindane are not known to occur as natural chemical products (WHO 1979a).However, since levels of concentration for most isomers of BHC, and specifically lindane, have been reported in a variety of environmental media, the potential for exposure to humans and animals has been established. Residues of BHC and lindane have been detected in air, water and sediments, and soil, as well as in food and drink. Residues have also been observed in animals and humans. One of the metabolites of lindane is hexachlorobenzene (HCB). It has been observed that lindane is made aromatic in the rat, yielding HCB both in vitro and in vivo. However, the precise mechanism of the biotransformation reaction of lindane to HCB is not known (Gopalaswamy and Aiyar 1986). Currently, the potential for exposure to BHC is believed to be almost nonexistent in the U.S. Domestic use ofBHC has been halted, and all products were reformulated to incorporate 99% pure qamma isomer. While residue levels of the alpha, beta, and delta isomers of BHC in domestic commodities have been reduced considerably, some residues will most likely remain because of the persistence of these isomers and the continued use of lindane (U.S. EPA 1985a). These actions undertaken in the U.S. have reduced the possibility of future human exposure to the other isomers of BHC; however, exposure to lindane is possible since lindane is still used as a human medicinal, as well as in a variety of other consumer products (U.S. EPA 1985a). Humans are exposed to lindane primarily through ingestion and also through dermal and inhalation exposure. The general environmental distribution, persistence, lipid solubility, and propensity for bioaccumulation of lindane make it more likely to be initially present in some food crops,

1979 1974-76

1973 1977 1974 1974 1974 1976 1976 1981 1981 1974 1974-75 1979

Italy Italy, Trento Italy Japan, Ehime (males) Japan, Ehime (females) Japan, Ehime (males) Japan, Ehime (females) Japan, Ehime (males) Japan, Ehime (females) Japan, Tokyo Japan, Osaka Japan, Osaka

1975 Spr 82-Spr 83 1982

Belgium W. Germany (children) India, Delhi India, Lucknow India, Lucknow (males) Iran

Geographical Area


28 29 126 20 23 22 23 46 46 30 59 32

60 48 340 6 50 170

No. of Samples

100

100

GLC-ECD HPLC GLC-ECD GLC GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GC-ECD GC-ECD GC-ECD GC-ECD GC-ECD GC-ECD GC GC-ECD GC-ECD

0.781b O.239 b 6.28 11.9 10.5 4.92 4.84 3.77 3.52 2.36 8.045 9.832

Analytical Method

0.76 0.15 10.11 b 2.334 2.536 0.26

Average Frequency Concentration (ppm) (percent)

Dejonckheere et al. (1978) Niessen et al. (1984) Ramachandran et al. (1984) Kaphalia and Seth (1983) Siddiqui et al. (1981) Hashemy-Tonkabonyand Soleimani-Amiri (1978) Leoni et al. (1978) Del Dot et al. (1978) Yamada et al. (1976) Mori et al. (1983) Mori et al. (1983) Mori et al. (1983) Mori et al. (1983) Mori et al. (1983) Mori et al. (1983) Fukano and Doguchi (1977) Yoshimura (1985) Yoshimura (1985)

Reference

Table 3. Levels of BHC (total) detected in human adipose tissue of the general population of various countriesa

(I>

.

3' 0

0

.... ....

t::I

0 ~

i:I 0.

I»

.P-

0 0

~

~

J'I 'tI

....~

~

~

:TJ

0\

-

0.30 0.31 0.29 0.33 0.48

91 157 201 236 994

1963-64

1965-67

1965-67

1969-71 1976-77 1962-66

0.43

43

1970-71 1965-66 1967-68 1971 1972 1984-85 1963-64

100 64

2.436 2.44 3.19 0.216 0.13 0.48 4.34 3.37 4.75 5.12 1.72 0.40

40 40 21 100 70 60 262 239 81 420 48 23

1984 1984 1971 1977-78

GLC GLC GLC

GLC

GLC

GLC

GC-ECD GLC GLC GLC GLC SH-TLC GC-ECD GC-ECD GC-ECD GC-ECD GC-ECD GLC

a Levels are reported as total BHC; the specific isomers were not isolated in these studies. bGeometric mean.

Japan, Osaka Japan, Osaka Japan Poland, Warsaw Poland, Lublin Pakistan Rumania Rumania Rumania Rumania Turkey, Ankara United Kingdom (females) United Kingdom (males) United Kingdom (females) United Kingdom (males) United Kingdom United Kingdom USA, Chicago Abbott et al. (1972) Abbott et al. (1981) Hoffman (1967)

Abbott et al. (1972)



Yoshimura (1985) Yoshimura et al. (1986) Doguchi et al. (1971) Syrowatka et al. (1979) Juszkiewicz and Stec (1971) Mughal and Rahman (1973) Aizicovici et al. (1974) Aizicovici et al. (1974) Aizicovici et al. (1974) Aizicovici et al. (1974) Karakaya and Ozalp (1987) Abbott et al. (1972)

-..J

.....

'"G

0

-e.0.

;I>

::s

~

a

::c r::

'" S·

G

r::

'"is.:

::c G

Italy, Trento Italy, Trento Italy Italy India, Calcutta India, Lucknow

Argentina Belgium Canada Canada Canada Czechos lovakia, Moravia W. Germany W. Germany (children) Holland

Geographical Area

1983-84 1973-74 Nov 75-0ct 86

1977

Spr 82-Spr 83

1975 1972 1976


29 4 26 28 100 6

11

78 282 48

52 60 168 99 29

No. of Samples

13

98 100

78 90

Frequency (percent)

0.193 b 0.006 b 0.l28 0.037 b 0.45 0.776

0.24 0.35 0.02" 0.10 b

0.09

N

VI

(l>

'"

0

Q.

-0'

>

::s

I»

8

~

'" S· ::t

(l>

~

'"s.:

98.4(1.00)

0.10(0.012) 0.13 (0.029)

0.10(0.13) 0.07 (0.023) 0.15 (0.026) 0.09 (0.009)

0.10 (0.013)

Race: White Non-white

Census Region: Northeastern North. central Southern Western

Entire nation

0.12 (0.013)

0.13 (0.018) 0.08 (0.023) 0.16 (0.027) 0.10(0.012)

0.11 (0.013) 0.14(0.019)

Parts per million, adjusted for lipid content of specimen.

98.4(0.99) 98.2 (1.29)

0.1 0 (0.0 12) 0.13 (0.015)

0.05 (0.009) 0.12 (0.011) 0.22 (0.018)

Median Amount (ppm)

1971

98.5(0.59)

97.4(1.17) 98.4(1.54) 99.8 (0.19) 97.8 (1.25)

98.3 (0.66) 100.0 ( -- )

97.8(0.90) 99.2(0.38)

96.6(1.49) 99.5 (0.36) 98.8 (0.83)

Percent Detected

Source~

U.S. EPA (1985b) (NHATS survey data).

b( __ ) Standard error cannot be calculated since the estimated percentage is 100%.

a

100.0 ( -- ) 94.7(3.03) 99.6(0.39) 100.0 ( -- )

0.10(0.015) 0.11 (0.012)

Sex: Male Female

97.4(1.88) 99.4(0.62)

0.04 (0.009) 0.10(0.010) 0.22(0.017)

96.1 (2.72) 98.8(0.88) 100.0 ( -- )

Percent Detected

0-14 15-44 45+

Age (in years):

Subpopulation

Median Amount" (ppm)

1970


0.09 (0.010)

0.Q7 (0.004) 0.09 (0.019) 0.14 (0.023) 0.06 (0.010)

0.09 (0.009) 0.12 (0.029)

0.08 (0.011) 0.11(0.012)

0.05 (0.009) 0.08 (0.008) 0.18 (0.018)

Median Amount (ppm)

1972

0.07 (0.010) 0.07 (0.011) 0.13 (0.028) 0.06 (0.012) 0.08 (0.010)

98.4(1.06)

0.08 (0.009) 0.08 (0.021)

0.08 (0.009) 0.09 (0.014)

0.06 (0.013) 0.06 (0.008) 0.17 (0.024)

Median Amount (ppm)

100.0 ( -- ) 98.8 (1.10) 100.0 ( -- ) 93.1 (3.95)

98.7(0.72) 96.5(3.25)

97.4(1.94) 99.3 (0.46)

95.8 (3.51) 98.6(0.79) l00.0( --)

Percent Detected

1973

100.0 ( -- )

100.0 ( -- ) l00.0( --) l00.0( --) 100.0 ( --)

100.0 ( -- ) 100.0 ( --)

100.0 ( --) 100.0 ( --)

100.0 ( -- ) l00.0( --) 100.0 ( --)

Percent Detected

~

0

sa

t:C

-s·

:-0

0

Co

.PI» ::s

0 0

~

~

'i:j

.N

c

~

-

~

>Tj

0'1

N

27


Data from the NHA TS have been used to estimate population residue levels for the entire u.s. and for census regions and demographic categories by various subpopulations (U.S. EPA 1985b). These estimates are based on combined data for fiscal years 1970 to 1983 for the presence of beta-BHC in the U.S. population. A statistical data analysis of the NHA TS survey was performed to determine baseline estimates for beta-BHC in adipose tissue and time trends for these concentrations. This analysis found the median residue level at 0.14ppm beta-BHC for the entire nation. The baseline levels vary across the different geographic areas and demographic groups. For the median levels, the levels increase with age, and the South Census Region had a higher median level than all the other census regions. The analysis also indicated: (1) there are no differeces in subpopulations with respect to the percentage of individuals having detectable levels of beta-BHC, and (2) the '0-14 years' age group has a lower percentage of individuals having quantifiable levels of beta-BHC. No other differences exist among subpopulations. Table 8 provides the separate baseline estimates for each survey year from 1970 to 1983 by subpopulation. This table shows that the baseline levels for the median residue amounts have decreased considerably for years 1981 and 1983 compared with previous years. A comparison of the subpopulations separately shows that there is a consistent increase in beta-BHC levels with age group for each year, but the levels do not differ by sex or race. The South Census Region has much higher median levels than the others. Figure 2 provides the geometric mean levels of beta-BHC for years 1970-83 for the U.S. population. A time trend analysis was done for beta-BHC for different distribution characteristics for the same survey years. The analysis showed that the national trends indicate the percentage of the population with detectable

r: ---\/.~.__

{-

0.40

f

0.20

;;-

0.15

"i

T

._.

~

.-.-.~

0.10 0.05 0.00

.-.

+----+---+----+---+----+--+---+--+---+--+----1 1970

1971

1972

1973

1974

1975

1978

1977

1978

1979

1981

SUMIY (FIscal) Yea,

Fig. 2. National Human Adipose Tissue Survey (lipid adjusted): beta-BHC.

1983

28


levels of beta-BHC remains near 100% and that the median level is estimated to be decreasing. It also indicated that the percentage of persons with quantifiable levels of the beta isomer was decreasing and the average beta-BHC concentration has decreased from 0.45 ppm in 1970 to approximately 0.16 ppm since 1981.

IV. DDT and Related Compounds 1,1,1-Trichloro-2,2' -bis(p-chlorophenyl)ethane (DDT) (the acronym stands for dichlorodiphenyltrichloroethane its earliest chemical name) is a broadspectrum, persistent insecticide. Under most environmental conditions, especially in soil and water, DDT is a stable compound. The persistence of DDT is mainly due to its very low water solubility and its high lipophilicity. Some of the metabolites of DDT, most notably DDE (1,1,-dichloro-2,2'-bis(pchlorophenyl)-eth ylene) and D D D (1, 1-dichloro-2,2'-bis(p-chlorophenyl)ethane), are as stable and persistent in the environment as DDT (WHO 1979b; U.S. EPA 1980a). DDT was first synthesized in Germany in 1874, but its insecticidal properties were not realized until 1939. The insecticidal properties of DDD were originally discovered in 1944, and its commercial use began in 1945. The primary uses of DDT have been agricultural, residential, and institutional. It has been used for the control of insect pests in gardens, fields, forests, and orchards, especially on cotton, soybean, and peanut crops. DDT continues to be used extensively worldwide in public health programs as a mosquito larvicide, as a residual spray for the eradication of malaria in dwellings, and as a dust in human delousing programs for the control of typhus. In addition, DDT has been used for mothproofing fabrics (WHO 1974). It was also used for agricultural purposes in many foreign countries including the Federal Republic of Germany, Egypt, Italy, Sudan, and Colombia. Along with its use as an insecticide, DDD was used as a therapeutic drug (Hayes 1982; WHO 1974). In the U.S., the use of DDT increased significantly until 1959 and then steadily declined until 1972. Its agricultural use was canceled by the U.S. EPA in 1972; since then, the use of DDT in the U.S. has been effectively discontinued. The use of DDD was prohibited in Switzerland in 1972, and its use was restricted in the U.S.S.R. (WHO 1979b). In addition, other countries have restricted or banned the use of DDT except when it is needed for the protection of health. In some tropical countries, DDT is still used for vector control. DDT and/or its derivatives have been found in most environmental media, including air, rain, soil, water, plants, animals, and food. These chemicals have also been found in human tissues, most notably adipose, and in human blood and milk.


29

The primary route of exposure of humans to DDT has been through the ingestion of small amounts in the diet. Meats, fish, poultry, and dairy products are the primary sources of DDT residues in the human diet (U.S. EPA 1980). After inhalation and ingestion, DDT can be absorbed from the respiratory or gastrointestinal tract. Dermal absorption of DDT is very limited. In humans, DDT is first dechlorinated to DDD and then is either metabolized to the metabolite DDA or excreted directly as DDD. DDA is water soluble and excretable, and thus is readily eliminated in conjugated form from the body through urine (Kutz et al. 1974a). DDE storage in the body is primarily a result of ingesting DDE previously degraded in the environment from DDT rather than the result of ingesting DDT (Kutz et al. 1974a; WHO 1974; Hayes 1982). DDT and DDE have high fatwater partition coefficients. Therefore, they tend to accumulate in the adipose tissue of both humans and animals. Laboratory studies indicate that following exposure, DDT is slowly eliminated from the body, usually in the form of one of the metabolites. During the late 1950s and early 1960s, average storage of DDT in fat was approximately 5 ppm and a total of 15 ppm for DDT-derived materials. However, with the decline in use of DDT the average levels of DDT in adipose tissue decreased to about 1 to 2 ppm and a total of about 9 ppm for DDT -derived materials (Murphy 1986). Therefore, restriction on the use of DDT led to lower concentrations in food products, thus promoting a decline in body burden of DDT derivatives in the general population. The general population has sustained exposure to DDT and its derivatives. Practically every person since the mid-1940s, when DDT was first used commercially, has had some exposure to the tissue storage of DDT (Murphy et al. 1986). Numerous studies, performed both domestically and abroad, have measured the levels of DDT and its derivatives in the adipose tissue of the general population. These studies are summarized in Tables 9-11. Studies were conducted by Davies et al. (1969) and by Kutz et al. (1977a) on the racial stratification of organochlorine insecticide residue in human adipose tissue. Davies et al. (1969) reported diverse stratification of DDE level due primarily to race differences. The median level of samples from blacks (9.6 ppm) was approximately twice that of DDE levels in samples from whites (4.9 ppm). In the study of Kutz et al. (1977a) the most marked case of racial difference in residue level was total DDT equivalents. The geometric mean of samples from blacks (8.33 ppm) was almost twice that of DDT samples from whites (4.65 ppm) (Kutz et al. 1977a). Figure 3 presents data compiled from the NHA TS for fiscal years 1970-83, showing a steady decrease in the concentration of DDT in adipose tissue levels of the general population of the U.S. Most uses of DDT were canceled in the U.S. in 1973, and the levels of this chemical and its metabolites have shown a sharp decline. The data

Belgium Belgium Canada, Ontario Canada, Ontario Canada, Ontario Costa Rica Czechoslovakia, Moravia Denmark Finland Finland France W. Germany W. Germany (children) W. Germany, Rostock Holland Holland India India, Delhi India, Delhi India, Culcutta

Geographical Area

1982 1976

1979

Spr 82-Spr 83 1979 1969

1980-81 1972-73 1983

1969 1975 1969-70 1971-72 1973-74 Oct 81-Feb 82

11 50 14 340 100

48 70

282

78 82 105 73

37 282 129 30

60

100

100

100 95

100

4.9 4.00 1.75" 3.920 4.68 15.43" 0.46

0.57 b

12.33 4.8" 0.33 2.51 3.27 1.1

9.7 8.29 7.59 5.67 3.69 59.28

Total DDT

Average Date of Sample No. of Frequency Concentration Collection Samples (percent) (ppm)

GE-ECD

Nonhydro. GLC-ECD

HPLC GC

CGC

GLC-ECD GLC-ECD GLC-MS GLC-ECD

GLC-ECD

GLC-ECD

Analytical Method

Niessen et al. (1984) Luckas et at. (1981) Wit (1971) de Vlieger et at. (1968) Siddiqui et at. (1981) Bhaskaran et at. (1979) Ramachandran et at. (1984) Mukherjee et al. (1980)

Hruba et at. (1984) Kraul and Karlog (1976) Mussalo-Rauhamaa et al. (1984) Hattula et al. (1976) Fournier et al. (1972) Schulte (1975)

Wit (1971) Dejonckheere et at. (1978) Holdrinet et at. (1977) Holdrinet et at. (1977) Holdrinet et at. (1977) Barquero and Constenla (1986)

Reference

Table 9. Levels of DDT and total DDT detected in human adipose tissue in the general population of various countries

to.>

0 0

(1)

0

S·

t:C 0

-.

~

0

Co

::s

Il>

flo

~

~

'"tl

!'l

~

c

-

~

'TI

0

Italy, Trento Italy Italy Italy, Ferrara Japan Japan Japan Japan, Ehime Japan, Ehime Japan, Ehime Japan, Tokyo Japan Japan, Osaka Japan Japan Japan, Osaka Japan, Osaka Japan (females) Mexico, Torreon Mexico, Mexico City Mexico, Puebla New Zealand New Zealand Pakistan Pakistan

India, Lucknow (males) India, Lucknow Iran

1977 1973 1983-84 1966-69 1974 1979 1984 1974 1976 1981 1974 1974 1974-75 1976 1981 1979 1984 1971 1975 1975 1975 1973 1973 1970-71 1970-71

1979 1982 Sep 74-Nov 76

30 43 59 45 92 32 40 21 19 9 9 51 51 60 60

29 28 26 85 30 30 40

50 6 170

100 100

100

5.552a 8.55 a 0.8 9.262 5.156 5.631 2.240 7.49 4.46 3.84 3.59 7.12 4.52 4.44 3.84 4.267 1.99 3.60 21.47 8.31 3.44 0.70 6.36 25.0 25.0

3.920 1.75 8.13

GLC GLC GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD ColorimetricjTLC ColorimetricjTLC

GC-ECD GC-ECD GC-ECD GC GC-ECD GLC GC-ECD GC-ECD

GC GLC-ECD GLC-ECD GC-ECD

GC-ECD

GLC-TLC

(Continued)

Siddiqui et al. (1981) Kaphalia and Seth (1983) Hashemy-Tonkabonyand Soleimani-Amiri (1978) Del Dot et al. (1978) Leoni et al. (1978) Focardi et al. (1986) Prati et al. (1972) Yoshimura (1985) Yoshimura (1985) Yoshimura (1985) Mori et al. (1983) Mori et al. (1983) Mori et al. (1983) Fukano and Doguchi (1977) Mori et al. (1983) Yoshimura et al. (1979) Mori et al. (1983) Mori et al. (1983) Yoshimura et al. (1981) Yoshimura et al. (1986) Doguchi et al. (1971) Albert and Mendez (1980) Albert and Mendez (1980) Albert and Mendez (1980) Solly and Shanks (1974) Solly and Shanks (1984) Mughal and Rahman (1973) Mughal and Rahman (1973)

C1>

w

'"C1>

-e' 0

:> Q..

::s

'"

3

::t \:

S·

[Jl

C1>

[Jl

s.: \:

:;:Q

Poland, Lublin Rumania Rumania Rumania Rumania Turkey, Ankara United Kingdom (males) United Kingdom (females) United Kingdom (males) United Kingdom (females) United Kingdom United Kingdom USA, California USA, Tallahassee, FL USA, Savannah GA, and Wenatchee, W A USA, Atlanta, GA USA, Wenatchee, W A USA, Chicago, IL USA, California

Geographical Area

43 23 157 91 201 236 75 49 61 36 28 282 25

1963-64

1963-64

1965-67

1965-67 1969-71 1976-77 1951 1956

1958

1963 1964 1951

70 262 239 81 420 48

1965-66 1967-68 1971 1972 1984-85

100

4.9 5.5 2.4 2.6 5.3

2.5 2.5 2.6 5.3 7.4

3.3

2.7

3.7

4.08 17.34 16.90 11.94 3.33 7.12

Average Date of Sample No. of Frequency Concentration (ppm) Collection Samples (percent)


Colorimetric Colorimetric GLC GLC Colorimetric

GLC GLC GLC Colorimetric Colorimetric

GLC

GLC

GLC

GC-ECD

GLC

Analytical Method

Durham Durham Durham Durham Durham

(1969) (1969) (1969) (1969) (1969)

Abbott et ai. (1972) Abbott et al. (1972) Abbott et al. (1981) Durham (1969) Durham (1969)




luszkiewicz and Stec (1971) Aizicovici et al. (1974) Aizicovici et al. (1974) Aizicovici et al. (1974) Aizicovici et al. (1974) Karakaya and Ozalp (1987)

Reference

w

n

0

...

3

0

...t:Pa.

~

0

Po

::l

Po>

.P-

0 0

~

~

."

= F

~

~

'T1

N

USA, Tallahassee, FL USA, Savannah, GA, and Wenatchee, W A USA, Atlanta, GA USA, Atlanta Louisville, Phoenix, and Wenatchee USA, Idaho USA, Texas USA, Tucson, Arizona USA, Hawaii USA, Miami USA, Wenatchee, W A USA, Chicago, IL USA (general pop.) USA, New Orleans LA USA, Dade Co., FL USA, Utah USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) 61 36

130 200 221 70

28 282 64 25 42 103 1412 1616 1920 1092 898

1958

1965 1970 1969-72 1967-68

1963 1965 1965 1965

1967-71 1970 1971 1972 1973 1974 1975 1976 1977 1978 1979 1981 1983

49

1956

99.83 99.75 99.95 100 100

100

5.89" 5.02" 4.76" 4.35" 3.14" 3.52" 3.10" 2.24" 1.67"

6.88"

12.7 1.9 23.18 1.54 1.30 2.81 6.7 11.1 7.6 10.3 10.56 7.31 7.88" 7.95"

11.7 15.6

19.9

GLC GLC GLC GLC GC-ECD GC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD

Colorimetric GLC-ECD GLC-ECD

Colorimetric Colorimetric

Colorimetric

(Continued)

Durham (1969) Wyllie et al. (1972) Burns (1974) Morgan and Roan (1970) Morgan and Roan (1970) Morgan and Roan (1970)' Durham (1969) Durham (1969) Durham (1969) Durham (1969) Fiserova-Bergerova et al. (1967) Warnick (1972) Kutz et al. (1977) Kutz et al. (1977b) Kutz et al. (1977b) Kutz et al. (1977b) Kutz et al. (1977b) US EPA (1986) (unpub.) USEPA (1986) (unpub.) USEPA (1986) (unpub.) USEPA (1986) (unpub.) USEPA (1986) (unpub.) USEPA (1986) (unpub.) USEPA (1986) (unpub.)

Durham (1969) Durham (1969)

Durham (1969)

w w

C1>

fIl

0

-e.

> Q..

::s

Ei" :I: ~ 8~

fIl

C1>

~

fIl

s:

:;1:1 C1>

Argentina Belgium Belgium Canada Canada Canada Canada, Kingston Canada, Ottawa Costa Rica Czechoslovakia, Moravia W. Germany (children)

USA, Atlanta, Louisville, Phoenix, and Wenatchee USA, Hawaii USA USA, New Orleans, LA USA, Dade Co., Fl USA, Chicago, IL USA, Texas Zaire

Geographical Area

78 48

Nov 79-Jan 81 Nov 80-Jan 81 Oct 81-Feb 82

1980-8i

Spr 82-Spr 83

60

52 70

130 30 64 25 42 994 35

168 99 29 91 84 30

1975 1972 1976

1965 1968 1965 1965 1965 1962-66 1983 1983

100

99 98 97

100 100

0.08 b

3.60

p,p'-DDT 1.53 3.8 1.52 0.439 0.311 0.442 0.159 0.128 12.08

4.0 1.16 2.5 2.3 2.81 2.6 1.67 b 62.45



HPLC

GLC-ECD

GLC-ECD GC-MS GC-TLC-MS GLC-MS GC-ECD GC-ECD GLC-ECD

Colorimetric GLC GLC GLC GLC-ECD GLC-ECD GC

Analytical Method

Niessen et al. (1984)

Hruba et al. (1984)

Garcia Fernandez (1971) Van Haver et al. (1978) Dejonckheere et al. (1978) Mes et al. (1977) Mes et al. (1982) Mes et al. (1985) Williams et al. (1984) Williams et al. (1984) Barquero and Constenla (1986)

Durham (1969) Casarett et al. (1968) Durham (1969) Durham (1969) Fiserova-Bergerova et al. (1967) Hoffman et al. (1967) Adeshina and Todd (1988) Okond'Ahoka (1984)

Reference

('I)

0

..,

S·

0 .... ....

IX'

~

tl

Co

P. I» ::s

0 0

~

;:c

"C

•N

~ ....

~

~

'Tl

w .,..

Warsaw, Poland Turkey, Ankara United Kingdom (males)

Italy Italy, Ferrara Italy, Trento Italy, Trento Italy Japan (females) Japan Japan Japan Japan Japan, Tokyo Japan, Osaka Mexico, Terreon Mexico, Mexico City Mexico, Puebla Pakistan Poland

Holland India, Delhi India, Delhi India, Lucknow (males) India, Lucknow Iran

11

100 48 43

1963-64

3

60

26 85 30 29 28 21 241 30 30 40 30 32 19 9 9

50 6 170

50 340

1977-78 1984-85

1974 1979 1984 1974 1979 1975 1975 1975 1970-71

1977 1973-74 1971

1983-84 1966-69

1979 1982 Sep 74-Nov 76

1979 1982

100

63 89 55 100

92.9 97 100

100

100

1.2

1.011 0.62

0.83 1.485" 2.2" 0.878" 1.487" 0.96 0.54 0.755 0.390 0.240 0.68 0.480 0.82 1.08 0.48 11.4 1.424

1.565 0.467 2.64

0.29" 1.565 5.78"

GLC

GC GC-ECD

GLC-ECD GLC-ECD GLC-ECD Colorimetric/TLC GC-ECD

GC

GC-ECD GC-ECD GLC GC GLC-ECD GLC GC-ECD

GC-ECD

GLC-ECD

Nonhydro. GLC-ECD GC-ECD


(Continued)

Siddiqui et al. (1981) Kaphalia and Seth (1983) Hashemy-Tonkabonyand Soleimani-Amiri (1978) F ocardi et al. (1986) Prati et al. (1972) Prati and Del Dot (1971) Del Dot et al. (1978) Leoni et al. (1978) Doguchi et al. (1970) Curleyet al. (1973) Yoshimura (1985) Yoshimura (1985) Yoshimura (1985) Fukano and Doguchi (1977) Sugiyama et al. (1981) Albert and Mendez (1980) Albert and Mendez (1980) Albert and Mendez (1980) Mughal and Rahman (1973) Szymczynski and Waliszewski (1981) Syrowatka et al. (1979) Karakaya and Ozalp (1987)

de Vlieger et al. (1968) Siddiqui et al. (1981) Ramachandran et al. (1984)

v.

w

06· 0 n '"

> Q.

::l

I'>

El

=: 1=

Ei"

n

= '"

'" s.:

n

\ltj

Argentina Canada Canada Canada

United Kingdom (females) United Kingdom (males) United Kingdom (females) United Kingdom United Kingdom USA, Monroe, LA USA, Monroe, LA USA, Dade Co., FL USA, Dade Co., FL (females) USA, Hawaii USA, Monroe, LA USA, Texas USA, Texas USA, Utah USA, Idaho

Geographical Area

91 201 236 22 8 42

1965-67 1969-71 1976-77 1977 1980

1976

1972

1984 1969-72 1987-88 1967-71 1970

157

1965-67

52 168 29 99

10 30 10 221 35 103 200

23

1963-64

96

100

70 100

100

50

0.40 0.031 0.039 0.032

GC-MS GLC-MS GC-TLC-MS

GC-ECD GC-ECD GLC-ECD GLC-ECD GC GC-ECD GC-ECD

0.81 1.16 0.70 3.48 0.294b 1.53 1.9 o,p'-DDT

GLC GLC GLC GLC GLC-ECD GC-ECD

GLC

GLC

Analytical Method

0.68 0.52 0.21 1.27 0.82 2.81

0.83

1.0



Garcia Mes et Mes et Mes et

Fernandez (1971) al. (1977) al. (1985) al. (1982)

Barquet et al. (1981) Casarett et al. (1968) Holt et al. (1986) Burns (1974) Adeshina and Todd (1988) Warnick (1972) Wyllie et al. (1972)

Abbott et al. (1972) Abbott et al. (1972) Abbott et al. (1981) Greer et al. (1980) Holt et al. (1986) Fiserova et al. (1967)



Reference

(1)

0 ....

0

~

-S·

tl ~

::I 0.

~

P-

0 0

~

;t

'"C

.N

c

~

-

~

'Tj

w

0"-

'Geometric mean. bMedian.

Poland, Warsay USA, Idaho USA, Texas USA, Texas

Costa Rica W. Germany W. Germany (children) India, Delhi Italy, Trento Italy Japan (females) Japan New Zealand Poland

1977-78 1970 1969-72 1987-88

1973

100 200 221 35

48 340 18 28 21 241 51 3

Spr 82-Spr 83 1982

1973-74 1971

30 282

Oct 81-Feb 82

84 89 81

100

58

78

97

0.082 0.1 0.24 0.014b

Trace 1.810.090.0460.11 b 0.08 0.70 0.291

0.70 0.044

GC GLC-ECD GLC-ECD GC

HPLC GC-ECD GLC GLC-ECD GLC GC-ECD GLC-ECD GC-ECD

GLC-ECD

Niessen et al. (1984) Ramachandran et al. (1984) Prati and Del Dot (1971) Leoni et al. (1978) Doguchi et al. (1970) Curley et al. (1973) Solly and Shanks (1974) Szymczynski and Waliszewski (1981) Syrowatka et al. (1979) Wyllie et al. (1972) Burns (1974) Adeshina and Todd (1988)

Barquero and Constenla (1986) Schult et al. (1975)

-...I

W

'"0

0

>6'

> Co

::s

I»

= 8

X

'"5'

0

s:'" =

~ 0

170

85 29

1979 1982

1974-76

1966-69 1977

Iran

Ital y, Ferrara Italy, Trento

11

78 73 282 48 6 50 340

1975 Spr 82-Spr 83

1980-81

Czechoslovakia, Moravia Finland W. Germany W. Germany (children) Holland India, Lucknow India, Lucknow (males) India, Delhi

Nov 79-Jan 81 Nov 79-Jan 81 Oct 81-Feb 82

1972 1976

60 73 168 99 29 91 84 30

1975

Belgium Belgium Canada Canada Canada Canada, Kingston Canada, Ottawa Costa Rica

No. of Samples 52


Argentina

Geographical Area

100 100

100 100 100

100

100 100 100

100 100

Frequency (percent)

GC-ECD GC

GC-ECD 5.26

6.l b 3.4U b

GLC-ECD GC-ECD

GLC-ECD GLC-ECD CGC HPLC Nonhydro.

GC-MS GC-MS GLC-MS GC-ECD GC-ECD GLC-ECD

GLC-ECD

Analytical Method

8.74 1.58 4.4 0.41" 1.26b 1.050 2.134 6.48 b

6.50 3.87 2.095 1.72 2.787 3.256 2.557 45.85

2.36

Average Concentration (ppm) Garcia Fernandez et al. (1971) Dejonckheere et al. (1978) Van Haver et al. (1978) Mes et al. (1977) Mes et al. (1982) Mes et al. (1985) Williams et al. (1984) Williams et al. (1984) Barquero and Constenla (1986) Hruba et al. (1984) Hattula et al. (1976) Schulte et al. (1975) Niessen et al. (1984) de Vlieger et al. (1968) Kaphalia and Seth (1983) Siddiqui et al. (1981) Ramachandran et al. (1984) Hashemy-Tonkabony and Soleimani-Amiri (1978) Prati et al. (1972) Del Dot et al. (1978)

Reference

Table 10. Levels of DDE detected in human adipose tissue in the general population of various countries

0

...0

S·

g=

~

0

Q..

::s

~

,p.

0 0

~

;z:

'tI

•N

~

...s:

~

'"Tj

\.U 00

1977-78 1984-85

1963-64 1963-64 1965-67 1965-67 1969-71 1976-77 1970 1967-68

Poland, Warsaw Turkey, Ankara

United Kingdom (males) United Kingdom (females) United Kingdom (males) United Kingdom (females) United Kingdom United Kingdom USA, Idaho USA, Tucson, AR USA, Hawaii 43 23 157 91 201 236 200 70

100 48

3

Poland

32 19 9 9 51 60 70

1979 1975 1975 1975 1973 1970-71

Japan, Osaka Mexico, Torreon Mexico, Mexico City Mexico, Puebla New Zealand Pakistan

31 26 21 241 30 30 40 30

Poland, Lublin

1974 1979 1984 1974

1983-84 1971

Italy, Trento Italy Japan (females) Japan Japan Japan Japan Japan, Tokyo

100

100

100

100 100 78 100 100

100

2.2 1.5 2.2 1.6 1.8 2.1 7.2 4.58 5.51

3.330 5.83

12.969

7.28

3.782 18.36 6.05 2.65 5.64 13.6

9.5 b 7.35 2.53 1.78 3.364 4.343 1.851 2.91

GLC GLC GLC GLC GLC GLC GLC-ECD GLC GLC

GC GC-ECD

GC-ECD

GLC

GLC-ECD GLC-ECD GLC-ECD GLC-ECD Colorimetric/TLC

GC

GC-ECD

GLC GC-ECD

(Continued)

Prati and Del Dot (1971) Focardi et al. (1986) Doguchi et al. (1971) Curley et al. (1973) Yoshimura (1985) Yoshimura (1985) Yoshimura (1985) Fukano and Doguchi (1977) Sugiyama et al. (1981) Albert and Mendez (1980) Albert and Mendez (1980) Albert and Mendez (1980) Solly and Shanks (1974) M ughal and Rahman (1973) Juszkiewicz and Stec (1971) Szymczynski and Waliszewski (1981) Syrowatta et al. (1979) Karakaya and Ozalp (1987) Abbott et al. (1972) Abbott et al. (1972) Abbott et al. (1972) Abbott et al. (1972) Abbott et al. (1972) Abbott et al. (1981) Wyllie et al. (1972) Morgan and Roan (1970) Morgan and Roan (1970) ~ (1)

::s

~

w

(1)

'"

0

..;'

0-

>

~

= s:: a

'" :r

s:: (1)

s:'"

b

a

Median. Geometric mean.

USA, Dade Co., FL USA, Dade Co., FL (females) USA, Monroe, LA USA, Chicago, IL USA, Monroe, LA USA, Monroe, LA USA, Utah USA, Texas

USA, Miami, FL USA, Hawaii USA, Tallahasse, FL USA, Savana, GA, and Wenatchee, WA USA, Atlanta GA USA, Louisville, KY, Phoenix, AR, and Wenatchee, WA USA, Texas USA, Wenatchee, WA USA, Chicago, IL USA, NE, Mid W., Deep S., and Far W. USA, New Orleans, LA USA, Dade Co., FL

Geographical Area

10 22 994 8 10 103 35

1977 1962-66 1980 1984 1967-71 1987-88

64 25 42

1965 1965

125

130 221 28 282

1965 1969-72 1963 1964

1967-68

61 36

30 49

No. of Samples

1958

1956


100 100

100

8

100

Frequency (percent)

5.91 6.85 7.0 9.58 3.42 5.03 0.343 b

7.3"

5.1 8.0 6.67

8.7 17.37 2.4 8.2

6.8 10.1

6.67 4.48 12.5



GC-ECD GLC GLC GLC-ECD GLC-ECD GC-ECD GC

GLC GLC GC-ECD

Colorimetric GLC-ECD GLC GLC

Colorimetric Colorimetric

GLC GC-ECD Colorimetric

Analytical Method

Barquet et al. (1981) Greer et al. (1980) HolTman (1967) Holt et al. (1986) Holt et al. (1986) Warnick (1972) Adeshina and Todd (1988)

Durham (1969) Durham (1969) Fiserova-Bergerova et al. (1967) Davies et al. (1969)

Durham (1969) Burns (1974) Durham (1969) Durham (1969)

Durham (1969) Durham (1969)

Morgan and Roan (1970) Casarett et al. (1968) Durham (1969)

Reference

(1)

....

0

S·

= 0 .... ....

cO ~

::I

I"

P.

0 0

~

P::

'tl

•N

= ....

~

~

'Tl

~

0

b

a

Median. Geometric mean.

Mexico, Torreon Mexico, Mexico City New Zealand Japan, Osaka Poland, Lublin Poland, Warsaw USA, Dade Co., FL USA, Texas USA, Monroe, LA USA, Hawaii USA, Monroe, LA USA, Monroe, LA

Belgium Canada Canada, Kingston Canada, Ottawa Costa Rica W. Germany W. Germany (children) Japan Japan Japan Japan India, Lucknow Iran

Geographical Area

1980 1984

1969-72 1977

1977-78

1975 1975 1973 1979

1974 1979 1984 1979 1974-76

Spr 82-Spr 83

1975 1972 Nov 79-Jan 81 Nov 80-Jan 81 Oct 81-Feb 82


19 9 51 32 70 100 42 221 22 30 8 10

60 168 91 84 30 282 48 241 30 30 40 50 170

No. of Samples

50 100

93

11 41

47 89 29

70

26 67 37.5 73

Frequency (percent)

0.l6 0.44 0.07 0.004 0.003 0.049 0.28 0.10 0.09 b 0.018 0.48 0.21

0.27 0.006 0.014 0.009 0.63 0.Q25 0.01' 0.04 1.008 0.898 0.150 0.221 0.232


GLC GC GC-ECD GLC-ECD GLC GC-ECD GLC-ECD GLC-ECD

GLC-ECD GLC-ECD GLC-ECD

GLC-TLC GC-ECD

HPLC GC-ECD

GLC-ECD GC-MS GC-ECD GC-ECD GLC-ECD

Analytical Method Dejonckheere et al. (1978) Mes et al. (1977) Williams et al. (1984) Williams et al. (1984) Barquero and Constenla (1986) Schulte et al. (1975) Niessen et al. (1984) Curley et al. (1973) Yoshimura (1985) Yoshimura (1985) Yoshimura (1985) Siddiqui et al. (1981) Hashemy-Tonkabonyand Soleimani-Amiri (1978) Albert and Mendez (1980) Albert and Mendez (1980) Solly and Shanks (1974) Sugiyama et al. (1981) Juszkiewicz and Stec (1971) Syrowatta et al. (1979) Fiserova-Bergerova et al. (1967) Burns (1974) Greer et al. (1980) Casarett et al. (1968) Holt et al. (1986) Holt et al. (1986)

Reference

Table 11. Levels of DDD detected in human adipose tissue in the general population of various countries

0

~ .....

'"0

0

-e.

:> p..

::s

s::

::t: 3po

'" S·

0

s:'"s::

:;:g

42 ,.

~ ~

'"

~

n

~

..,..,

F.W. Kutz, P.H. Wood, and D.P. Bottimore 900 8.00 7,00

600 5.00 4,00

300

3

200

100 000 1970

1971

1972

1973

1974

1975

1976

1977

1978

1979

1001

1983

Survey (Fiscal) Year

Fig. 3. National Human Adipose Tissue Survey (lipid adjusted): total DDT.

in Fig. 3 reflect a decline in the mean concentration from approximately 8 ppm in 1970 to about 2 ppm in 1983.

v.

Heptachlor/Heptachlor Epoxide, Chlordane/Oxychlordane, trans- N onachlor

Heptachlor was isolated from technical chlordane in 1946. It is known chemically as 1,4,5,6,7,8,8-heptachloro-3a,5,7,7a-tetrahydro-4,7-methano1H-indene. Technical heptachlor contains about 72 to 74% of heptachlor, 20 to 22% of gamma-chlordane, and 4 to 8% of gamma-nonachlor (WHO 1988a). Heptachlor epoxide is a biological oxidation product of heptachlor that is formed by some plants and animals, including humans, after exposure to heptachlor (Dynamac 1987b). Chlordane is known chemically as 1,2,4,5,6,7,8,8-octachloro-2,3,3a,4,7,7ahexahydro-4,7-methano-lH-indene. Technical chlordane is a mixture of at least 26 different chemical components, including alpha- and gammachlordane and heptachlor (WHO 1988b). Oxychlordane is a metabolic intermediate of chlordane that results from oxidative reactions. It can be further converted to other key metabolites. trans-Nonachlor (1,2,3,4,5,6, 7, 8, 8a-nonachlor-3a,4, 7, 7a-tetra-hydro-4, 7methanoindane), is a component of technical chlordane and technical heptachlor (Kutz et al. 1976). trans-Nonachlor is also reported to be a metabolite of chlordane (WHO 1979a). Each of the subject chemicals is a chlorinated cyclodiene. Chlordane and heptachlor were registered in the U.S. under the early Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA), then administered by the U.S. Department of Agriculture, in the late 1940s and early 1950s. Use of these


43

insecticides has resulted in environmental contamination. Heptachlor epoxide, oxychlordane, and trans-nonachlor are also environmental contaminants as a result of the use of heptachlor and/or chlordane. These chlorinated cyclodienes are very persistent in the environment and have been reported to remain biologically active for more than 30 yr after application (U.S. EPA 1987a). Although these chemicals are persistent and relatively immobile in the soil, they are volatile, and some volatilization occurs from the soil to the air. Monitoring data have shown that residues of the cyclodienes, especially their metabolites, ha ve been detected throughout the food chain and in most human tissues examined (US EPA 1987a; WHO 1988b). High levels of heptachlor epoxide have been found in the general population, particularly in areas of high human exposure (WHO 1988a). Residues were also found in water and sediment, as well as in tissues of birds, fish, and wildlife species (U.S. EPA 1987a). In the U.S., manufacturers have voluntarily canceled the registration of products containing heptachlor and chlordane. Former uses of heptachlor in the U.S. include foliar, soil, and structural applications and the control of mosquitos. Its domestic use in the 1970s and 1980s was confined almost exclusively to the control of soil insects and termites (WH 0 1988a; U.S. EPA 1987a). Chlordane was used as a broad-spectrum, contact insecticide, for more than 35 yr. Employed mainly for nonagricultural purposes, primarily for the protection of structures, it was also used on lawns and turf, ornamental trees, and drainage ditches (WHO 1988b). The use of heptachlor has been restricted or prohibited in some foreign countries as well. European Community Legislation prohibits the marketing and use of plant protection products that contain heptachlor. The use of heptachlor for agricultural purposes is prohibited in countries such as the German Democratic Republic, Japan, the USSR, Finland, and Ecuador, to name a few. The registration of these products was discontinued in Canada in 1985 (WHO 1988a). The use of chlordane is prohibited in a number of countries, including Argentina, Finland, Sweden, Switzerland, the USSR, and the German Democratic Republic. By 1985, Canada has limited the registration of chlordane to its use as a restricted class termiticide (WHO 1988b). Previous exposures to these parent chemicals resulted primarily from ingestion of food that had been treated with the insecticide and from inhalation of the interior air of buildings that had been treated with the termiticide (U.S. EPA 1987a). However, food was the major source of exposure of the general population to chlordane and heptachlor. The use of chlordane and heptachlor decreased drastically in the U.S. in the 1970s after the EPA took regulatory actions resulting in the cancelation of virtually all uses except for subterranean termite control. Nevertheless, significant exposure to chlordane could have occurred in buildings where

Argentina W. Germany (children) USA, Dade Co., FL (females)

Geographical Area

Spr 82-Spr 83


10

52 48

No. of Samples 80

Frequency (percent)

Analytical Method HPLC GC-ECD

Average Concentration (ppm) 0.02 0.01" ND

Barquet et al. (1981)

Garcia Fernandez (1971) Niessen et al. (1984)

Reference

Table 12. Levels of heptachlor detected in human adipose tissue in the general population of various countries

@

o

S·

o

Cd

~

o

0-

§

p.

o o

~

p::

.~ 'tI

c

~

~

'TI

t

Belgium Belgium Canada Canada Canada Canada, Kingston Canada, Ottawa Costa Rica Finland Finland France W. Germany W. Germany (children) Holland Italy, Trento Italy, Trento Italy, Ferrara Italy Japan, Osaka Japan, Osaka Japan (females) Japan United Kingdom (males) United Kingdom (females) United Kingdom (males) United Kingdom (females)

Geographical Area

1965-67 1965-67 1969-71 1969-71

1966-69 1973-74 1974-75 1979 1971

1977

Spr82-Spr83

1083

Oct 81-Feb 82

1975 1972 1976


26 6 85 28 59 32 21 241 157 91 116 85

11

282 48

105

69 60 168 99 29 91 84 30

No. of Samples

92 100 90 19 61

85 95 83

100 100

Frequency (percent) 0.20 0.38 0.043 0.037 0.030 0.035 0.037 0.38 0.0023 0.002 0.32 0.092 0.02" 0.0085 b 0.042b 0.01 0.09 b 0.135 b 0.050 0.136 0.04 0.02 0.045 0.032 0.027 0.024


HPLC Nonhydro GC DLC GLC-ECD GLC-ECD GC GC GLC GC-ECD GLC GLC GLC

GLC-ECD

GLC-ECD GC-MS GC-MS GLC-MS GC-ECD GC-ECD GLC-ECD

Analytical Method

(Continued)

Van Haver et al. (1978) Dejonckheere et al. (1978) Mes et al. (1977) Mes et al. (1982) Mes et al. (1985) Williams et al. (1984) Williams et al. (1984) Barquero and Consten la(1986) Pyysalo et al. (1984) M ussalo-Rauhamaa et al. (1984) Fournier et al. (1975) Schulte et al. (1975) Niessen et al. (1984) de Vlieger et al. (1968) Del Dot et al. (1978) Prati and Del Dot (1971) Prati et al. (1972) Leoni et al. (1978) Yoshimura et al. (1979) Yoshimura et al. (1981) Doguchiet al. (1970) Curley et al. (1973) Abbott et al. (1972) Abbott et al. (1972) Abbott et al. (1972) Abbott et a\. (1972)

Reference

Table 13. Levels of heptachlor epoxide detected in human adipose tissue in the general population of various countries

:;g

.". VI

(1)

'"

0

.;'

> 0-

::l

'"

3

!:

::t:

'" S·

(1)

!:

'"s.:

(1)

"Median. bGeometric mean.

United Kingdom United Kingdom USA, Hawaii USA, Idaho USA, Texas USA, Monroe, LA USA, Monroe, LA USA, Monroe, LA USA, Dade Co., FL (females) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA, Texas Zaire

Geographical Area

1970 1971 1972 1973 1974 1975 1976 1977 1978 1979 1981 1983 1987-88

1970 1969-72 1977 1980 1984

1969-71 1976-77 201 236 30 200 221 22 8 10 10 1412 1616 1916 1092 898 779 682 789 827 796 384 407 35


100 100 100 94.76 96.23 90.29 97.71 96.33 95 97 96 95 95 91 93

97 98

Frequency (percent) 0.03 0.03 0.027 0.1 0.11 0.15 0.24 0.16 0.06 0.09 b 0.09 b 0.08 b 0.09 b 0.08 b 0.08 b 0.08 b O.07 b 0.07 b 0.07 b 0.09 b 0.09 b 0.086" 0.07



GLC GLC GLC GC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GC

Analytical Method Abbott et al. (1972) Abbott et al. (1981) Casarett et al. (1968) Wyllie et al. (1972) Burns (1974) Greer et al. (1980) Holt et al. (1986) Holt et al. (1986) Barquet et al. (1981) Kutz et al. (1976) Kutz et al. (1976) Kutz et al. (1976) Kutz et al. (1977) Kutz et al. (1977) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) Adeshina and Todd (1988) Okond' Ahoka et al (1984)

Reference

(I>

....

0

3·

.....

0

= .....

~

0

::s Q.

I'>

F-

0 0

~

:r::

'"C

F

~

~

~

"rl

.f:>. 0\


1979-81 1980-81 Oct 81-Feb 82 1983

Geographical Area

Canada, Kingston (alpha) Canada, Ottawa (alpha) Costa Rica (alpha) Finland (Chlor. Cpds) 91 84 30

No. of Samples 44 43 7

Frequency (percent) 0.018 0.016 0.01 0.007

Average Concentration (ppm) GC-ECD GC-ECD GLC-ECD

Analytical Method

Williams et al. (1984) Williams et al. (1984) Barquero and Constenla (1986) Pyysalo et al. (1984)

Reference

Table 14. Levels of chlordone detected in human adipose tissue in the general population of various countries

-..J

.".

n

'"

-e' o

> Co

::s

3I'>

!i '" S· ::t: s::

Co

~.

::c n

"Geometric mean.

Canada Canada Canada Canada (Kingston) Canada (Ottawa) Finland Italy USA USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA, Florida (females) USA, Texas

Geographical Area

1987-88

1971 1972 1973 1974 1975 1976 1977 1978 1979 1981 1982

1983 1973-74

1972 1976

Date of Sample Collection 168 99 29 91 84 105 83 27 951 1916 1092 898 779 682 789 827 796 384 407 10 35

No. of Samples

77.8 93.27 92.33 98.35 98.35 96.4 96.9 94.9 96.7 93.8 100 88 100

100 100

97 100

Frequency (percent) 0.055 0.055 0.063 0.042 0.039 0.002 0.053" 0.14 0.11 " 0.11" 0.12" 0.12" 0.11 " 0.11" 0.11" 0.11" 0.10" 0.09" 0.09" 0.19 0.09S"

Average Concentration (ppm) GC-MS GC-MS GLC-MS GC-ECD GC-ECD GLC-MS GLC-ECD GC-TLC-IR-MS GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GC-ECD GC

Analytical Method

Mes et al. (1977) Mes et al. (1982) Mes et al. (1985) Williams et al. (1984) Williams et al. (1984) Mussalo-Rauhamaa et al. (1984) Leoni et al. (1978) Biros and Enos (1973) Kutz et al. (1976) Kutz et al. (1976) Kutz et al. (1977a) Kutz et al. (1977a) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) Barquet et al. (1981) Adeshina and Todd (1988)

Reference

Table 15. Levels of oxychlordane detected in human adipose tissue in the general population of various countries

(1)

....

0

S·

0 .... ....

t:C

~

t:l

'0-::s"

F-

0 0

~

~

'tI

.N

c ....

~

~

'Tj

00

.j::>.

aGeometric mean.

USA, Florida-Dade Co. USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.) USA (general pop.)

Ca~ada

Finland

Geographical Area

1973 1974 1975 1976 1977 1978 1979 1981 1983

1983

Date of Sample Collection 102 19 10 1 49 779 682 788 826 796 384 407

No. of Samples

100 96 85 97 97 96 96 95 95

Frequency (percent) 0.004 0.056 0.35 > 0.1 a > 0.1 a O.OS" 0.12 a 0.09 a 0.12a O.12a O.04a 0.128

Average Concentration (ppm) GLC-MS GLC-MS GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD

Analytical Method

Mussalo-Rauhamaa et al. (1984) Mes et al. (1985) Barquet et al. (1981) Kutz et al. (1977a) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (un pub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (unpub.) U.S. EPA (1986) (un pub.) U.S. EPA (1986) (unpub.)

Reference

Table 16. Levels of trans-Nonachlor detected in human adipose tissue in the general population of various countries

~

"'

00

0

-6.

> Q..

::l

'"

3

s::

::z:

00

00

"'5: s:: "'S·

:;c


50

chlordane was used for other insect control as well as for termites. Moreover, in areas where heptachlor was used, inhaling dust or mist and drinking water from contaminated wells might also have accounted for exposure. Chlordinated cyclodienes are absorbed readily by humans following ingestion (food residues), and dermal and inhalation exposure. They are rapidly oxidized in animals by microsomal enzymes. The oxidized metabolites are stored in the adipose tissues, and elimination from the body is slow (WHO 1989; U.S. EPA 1987a; Hayes 1982). Heptachlor is oxidized by microsomal enzymes to heptachlor epoxide in mammals. Heptachlor epoxide, the most persistent metabolite, is formed rapidly and is found in the body, mainly in the adipose tissue (US EPA 1987a; Hayes 1982). Elimination usually takes place through the urine and feces. Human milk is also a route of excretion.

f

0.10

0.09

~ 0.08 ~ 0

~

0.07

0.06

"

0.05

"~

0.03

f

0.04

0.02 0.01

0.00 1970

1971

1972

1973

1974

1975

1976

1977

1978

1979

1981

1983

Fig. 4. National Human Adipose Tissue Survey: heptachlor epoxide.

i...

.'" ~ " ~

f !

0.15 0.14 0.13 0.12 0.11 0.1

•

0.09 0.08 0.07 0.06 0.05 0.04

0.03 0.02 0.01 1972

1973

1974

1975

1978

1977

1978

1979

1981

1983

Fig. 5. National Human Adipose Tissue Survey (lipid adjusted): oxychlordane.


51

Chlordane is believed to be metabolized by several oxidizing enzyme reactions; however, the metabolic pathway is complex, and not well understood. One of its major metabolites is oxychlordane. Oxychlordane has been found in the fatty tissues of rats and has been detected in the human adipose tissue sampled in the NHATS between 1970 and 1983. Levels of each of these cyclodiene chemicals have been reported in the adipose tissues of the general population, both in the U.S. and abroad. These levels are reported in Tables 12-16. Figures 4 and 5 present the levels of oxychlordane and heptachlor epoxide in the adipose tissues of the general population, as reported in the NHA TS data.

VI. HCB Hexachlorobenzene (HCB) is a ubiquitous chlorinated hydrocarbon, having been detected in most environmental media including air, water, plants, and soil, as well as in aquatic biota, mammals, and humans. It has been found by environmental monitoring studies in many countries. HCB enters the environment as an agricultural fungicide, and as an industrial byproduct formed in the production of chlorinated compounds. Chemically, HCB is a very stable compound, and persistent in the environment. Because of this persistence, specifically in the tissues of higher animals, and in the food chain, it continues to pose a threat to public health. HCB is no longer produced as a commercial product in the U.S.; it is found only as a waste byproduct in specific manufacturing processes. Since the mid 1970s, most HCB in the U.S. has been formed as a byproduct in the production of chlorinated solvents, pesticides, and other chlorinated compounds (Menzie 1986; US EPA 1986b). Five pesticides (i.e., pentachloro-nitrobenzene (PNCB), chlorothalonil, dimethyl-tetrachloroterephthalate (DCPA), picloram, and pentachlorophenol (PCP) have been identified as containing HCB in the technical grade products. In addition, some triazine herbicides were reported to contain low levels of HCB (US EPA 1986b). Domestically, the use of HCB is considered more historical than current because all uses have been essentially halted. In the U.S., the use of HCB for agriculture was fairly limited. Registered in 1972, HCB was used primarily as a seed protectant on grain and field crops, including barley, beans, corn, cotton, flax, oats, onions, peanuts, peas, sorghum, soybeans, rye, and wheat, but its principal use was to treat wheat seed for control of bunt. Since its registration, however, the use of HCB has been banned domestically, and its commercial production as an end product ceased in 1975. Other reported commercial uses ofHCB in the U.S. have decreased largely because of the diminishing supplies and development of acceptable

W. Germany W. Germany (children) Greece Ireland Italy Italy Japan Japan Japan

Czechoslovakia, Moravia Finland

1976 1981

1975 1973 1983-84

Spr 82-Spr 83

1980-81 1983

1972 1976 1979-81 1971-72 1973-74 1980-81 Oct 81-Feb 82

282 50 50 11 28 26 241 45 92

78 105

60 73 29 168 99 91 33 76 84 30

Belgium Belgium Canada Canada Canada Canada, Kingston Canada, Ontario Canada, Ontario Canada, Ottawa Costa Rica

1975

38


Australia

Geographical Area

100

100

100 97

100 100 100

63

Frequency (percent)

5.6 0.23" 3.84 0.15 0.896 b 2.26 0.08 0.13 0.065

8.41 0.02

1.36 0.97* 0.106 0.062 0.095 0.106 0.09 0.12 0.078 0.15

0.26


GLC-ECD GC-ECD GC-ECD GC-ECD GC-ECD

HPLC

GLC-ECD GLC-MS

GC-ECD GLC-ECD

GLC-MS GC-MS GLC-MS GC-ECD

GLC-ECD

Analytical Method Brady and Siyalia (1972) (cited in Hayes (1982) Dejonckheere et al. (1978) Van Haver et al. (1978) Mes et al. (1985) Mes et al. (1977) Mes et al. (1982) Williams et al. (1984) Holdrinet et al. (1977) Holdrinet et a1. (1977) Williams et a1. (1984) Barquero and Cons tenia (1986) Hruba et a1. (1984) Mussalo-Rauhamaa et a1. (1984) Schulte et a1. (1975) Niessen et a1. (1984) Abbott et a1. (1981) Abbott et a1. (1981) Leoni et a1. (1978) Focardi et a1. (1986) Curley et al. (1973) Mori et al. (1983) Mori et al. (1983)

Reference

Table 17. Levels of hexach lorobenzenc detected in human adipose tissue of the general population of various countries

~

0 .... CD

S·

;:::

0

I:C

:-c

tl

0-

::s

~

p..

0 0

~

;t

'i:I

.N

:::: ....

~

'Tl

tv

Vl

1971-72 1969-71 1976-77 1973 1974 1975 1976 1977 1978 1979 1981 1983

Switzerland United Kingdom United Kingdom USA USA USA USA USA USA USA USA USA USA, Dade Co., FL (females) Yugoslavia Zaire

"Median. bGeometric mean.

1977

Spain (urban)

1979-80 1983

1977

Spain, Barcelona Spain (rural)

10 15

12 201 236 1095 898 779 683 1025 947 908 402 200

28

171 12

51 3

New Zealand Poland

1973

15 38

Japan, Tokyo New Guinea

100

70.9 93.9 91.5 93.4 99.6 99.4 99.0 99.7 100.0

100

100 100

100

100 63

0.13 0.055 0.17

1.9 0.05 0.19 0.02b 0.04b 0.05 b 0.05 b 0.035 b 0.039 b 0.040 b 0.041b 0.031 b

1.08

5.55 0.84

0.31 0.128

0.21 0.26

GC-ECD GLC-ECD

GLC GLC GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-ECD

GC-ECD

GLC-ECD GC-ECD

GLC-ECD

Barquet et al. (1981) Jan (1983) Okond' Ahoka (1984)

Morita et al. (1975) Brady and Siyalia (1972) (cited in Hayes (1982) Solly and Shanks (1974) Szymczynski and Waliszewski (1981) To-Figueras et al. (1986) Pozo et al. (1978) (as cited in Hayes (1982)) Pozo et al. (1978) (as cited in Hayes (1982)) Abbott et al. (1981) Abbott et al. (1972) Abbott et al. (1981) Kutz et al. (1979) Kutz et al. (1979) Kutz et al. (1979) Kutz (1983) U.S. EPA (1986b) U.S. EPA (1986b) U.S. EPA (1989b) U.S. EPA (1986b) U.S. EPA (1986b)

w

VI

0

.;'

Co

I:l

':>"

::t c 3

5'

(I> Co

::s

I'>

3

c

::t

'" S·

c(1)

(1)

::c '"s.:


58 0.05

i.

0.04

"-

0.03

0

0.03

'"

~

n

f i

_---

0.04

0.02 0.02 0.01 0.01 0.00 1974

1975

1978

1977

1978

1979

1981

1983

Fig. 6. National Human Adipose Tissue Survey (lipid adjusted): hexachlorobenzene

banned and all registered products containing mirex were canceled in the U.S. Mirex is reported to have been used against leaf cutter ants in South America, harvester termites in South Africa, and mealybugs on pineapple in Hawaii. It was also investigated for use against yellow jackets in the U.S. (WHO 1979a). Mirex persists in the environment, and its residues have been detected in soil, water, food and drink, animals, and humans. Since this chemical has an affinity for lipids, it is stored and accumulated in the adipose tissue of animals and humans. The extensive production and use of mirex, along with its persistent nature, indicate that human exposure is wide-spread. Evidence of this exposure is shown by reports of its occurrence in the general environment and by its detection in human fat (WHO 1979a). A review of studies on human exposure to mirex has revealed detectable levels of this compound in human adipose tissue, and traces of mirex have been found in some human milk samples. During the period 1971-72, mirex was detected in the adipose tissues of six human subjects in the U.S., at levels ranging from 0.16 to 5.94 mg kg - 1. Although there appeared to be no evidence linking the positive identification of mirex to occupational exposure, these six subjects were all residents of those southern states where mirex had been used extensively for fire ant control (Kutz et al. 1974b). Average residues of mirex in the fat of residents in states where mirex has been applied were 1.32 mg kg- 1 fat (WHO 1979a). A special survey was initiated for the general population of the southeastern U.S. because of the evidence of mirex exposure reported by Kutz et al. (1974) (Kutz et al. 1985). Adipose tissue samples were taken from 40 sites randomly selected from eight southeastern states where mirex was

59


Table 19. Estimated percent positive detection of mirex and estimated mean levels of mirex residues

Variable

Geometric Mean (ppm) of Mirex, LEM-adjusted Estimated % Positive Positive Residues b Mirex Detection (Including Trace Values) N8 (Excluding Trace Values) N

All Age (in years) 0-14 15-44 ~45

Census division East-south central South atlantic West-south central Race Caucasian Non-caucasian Sex Male Female

10.2 ( 3.42)C

624

0.286 (0.048)

123

1.6 ( 1.37) 11.3 ( 3.66) 15.4(3.87)

70 229 325

0.172 (0.037) 0.283 (0.039) 0.297 (0.077)

8 47 68

37.6(10.94) 13.3 ( 3.06) 3.6 ( 2.57)

175 282 167

0.292 (0.018) 0.266 (0.083) 0.331 (0.049)

61 23 39

9.8( 4.28) 11.5 ( 4.02)

471 153

0.252 (0.030) 0.406 (0.102)

86 37

16.1 ( 5.16) 6.7( 2.79)

298 326

0.322 (0.085) 0.249 (0.023)

65 58

aN = Number of samples bLEM-Lipid-extractible materials. Calculation within the estimated percent positive. , Standard error. Source: Kutz et al. (1985).

used on a wide scale for fire ant control. The objective of this special study was to determine the prevalence and levels of mirex in the adipose tissue collected from areas treated with mirex. The data reviewed consisted of 624 observations for a weighted statistical analysis. The average minimum detectable quantity of mirex in human adipose tissue was within the range of 0.05 to 0.10 ppm. Approximately 1% of the target population was estimated to have trace amounts of mirex. Trace quantities were viewed as positive; however, trace mirex detections in the statistical analysis were not considered in the analysis of the quantifiable positive mirex levels. The results of the survey are presented in Table 19. The estimated positive mirex detection for the eight states was 10.2% and geometric mean in positive samples was 0.286 ppm. These findings are interpreted only as an indication of trends and patterns that may have existed in the population living in the eight-state mirex-treated region. Data from NHATS for the years 1971 to 1983, have shown that in less than 1% of the samples analyzed was mirex positively identified (US EPA

Geometric mean.

Nov 79-Jan 81 Nov 80-Jan 81 1977 1980 1984 1971-72 1975-76

Canada, Kingston Canada, Ottawa USA, Monroe, LA USA, Monroe, LA USA, Monroe, LA USA, Southern USA, Southeastern

a


Geographical Area 91 84 22 8 10 6 624

No. of Samples 65 30 91 100 20 100 10.20

Frequency (percent) 0.027 0.011 0.152 0.32 0.15 2.495 0.286"

Average Concentration (ppm) GC-ECD GC-ECD GLC-ECD GLC-ECD GLC-ECD GLC-MS GE-ECD

Analytical Method

Williams et al. (1984) Williams et al. (1984) Greer et al. (1980) Holt et al. (1986) Holt et al. (1986) Kutz et al. (1974b) Kutz et al. (1985)

Reference

Table 20. Levels of mirex detected in human adipose tissue in the general population of the USA and Canada

6

o

...!:Xlo S·

~

Q.

III

= o

~

o

~

P=

"'ti

F

~

~

'TI

g


61

1986, unpub.) Levels of mirex in the adipose tissue of the general population of Canada and the U.S. are shown in Table 20.

VIII. PCBs Polychlorinated biphenyls (PCBs) have been produced commercially in the U.S. since 1929. PCBs are chemically classified as halogenated aromatic hydrocarbons and are formed by the chlorination of a bi-phenyl molecule. Aroclor is a U.S. commercial mixture trade name used for some of the technical mixtures of a numbe,. of the individual congeners. There are 209 possible PCB congeners, and the physical and chemical properties of each congener vary according to degree and position of chlorination. However, all PCB compounds have low vapor pressures and low water solubility. PCBs were used in numerous industrial products prior to 1972. Because of their good chemical stability, insulating properties, and dielectric properties, PCBs have been widely used as coolants and lubricants in transformers, capacitors, and other chemical equipments. Other applications included their use in plasticizers, surface coatings, adhesives, inks, and pesticide extenders, as well as for microencapsulation of dyes in carbonless duplicating paper (WHO 1978; SRC 1987). PCBs were also reported to have been used in immersion oil for microscopes, as a catalyst carrier in the polymerization of olefines, in the conversion of waterpermeable solids to non permeable states, and in combination with insecticide and bactericide formulations. Mixtures of PCBs and chlorinated napthalenes were also used to insulate electric cables, and wires in mining and shipbuilding (WHO 1978). Twelve different types of aroclors were manufactured, with chlorine contents ranging from 21 to 68~.{,. PCBs are no longer manufactured or used industrially in the U.S. The industrial manufacture of PCBs ceased domestically in 1977 because they were discovered to be very persistent and to accumulate in the environment, potentially causing toxic effects. Even though PCBs are no longer produced in the U.S., exposure can still occur through continued in-place use of these compounds. For example, many of the transformers and capacitors that were filled with PCB-containing fluids during manufacture are still in service. Their useful lifetime can extend to 30 yr or more (SRC 1987). Because of the health implications of PCB exposure, some countries prohibited their production as early as 1972. Other countries limited their sale and use in dielectric fluids. PCBs are ubiquitous in the environment. They have been found in air, soil, water and sediments, food, and animals, as well as in human tissues and secretions (WHO 1978). The main sources of human exposure to PCBs are occupational and environmental. The major route of human exposure to

Austria Belgium Canada Canada Canada Canada Canada, Ontario Canada, Ontario Canada, Ontario Canada, Kingston Canada, Ottawa Denmark Denmark Finland Finland E. Germany W. Germany, Rostock W. Germany W. Germany (children) E. Germany Israel Italy

Geographical Area

28

48 282

70

1979

Spr 82-Spr 83

73 105

29 282 129 91 84 82

58 99 29 168

No. of Samples

1983

1969-70 1971-72 1973-74 Nov 79-Jan 81 Nov 80-Jan 81 1972-73

1972

1976


100

100 100 95

100

100

Frequency (percent) 4.6 1.45 0.944" 0.928" 0.907" 1.3 1.2 2.5 2.3 2.95 2.001 4.1h 5.0 1.97 0.26 6.2 3.5 8.0 0.67< 8.6 3.6 0.422


GLC-ECD

HPLC

GC

GLC-ECD GLC-MS

GC-ECD GC-ECD GLC-ECD

GLC-MS GLC-MS GLC-MS

Analytical Method

Zitko (1979) Van Haver et al. (1978) Mes et al. (1982) Mes et al. (1985) Mes et al. (1977) Zitko (1979) Holdrinet et al. (1977) Holdrinet et al. (1977) Holdrinet et al. (1977) Williams et al. (1984) Williams et al. (1984) Krau! and Karlog (1976) Zitko (1979) Hattula et al. (1976) Mussalo-Rauhamaa et al. (1984) Zitko (1979) Luckas et al. (1981) Zitko (1979) Niessen et al. (1984) Schulte et al. (1975) Zitko (1979) Leoni and D'Arca (1976)

Reference

Table 21. Levels of PCBs detected in human adipose tissue in the general population of various countries

I::

(I>

...0

t:x:I

......S·0

0 ~

Q..

::s

~

,p.

0 0

~

~

'"C

.N

...

~

~

'Tl

0'1 N

1260.

bGeometric mean. 'Median.

a Aroclor

Italy Italy Japan Japan, Ehime Japan, Tokyo Japan, Ehime Japan, Tokyo Japan Japan Japan Japan Japan, Ehime New Zealand New Zealand Norway Poland Poland, Warsaw United Kingdom United Kingdom USA, Monroe, LA USA, Monroe, LA USA Zaire 92 51

118 54 236

1981 1973

1974-75

1980 1984

1976-77 8 10

33 21 30 45 16 62 32 40

1971-72 1973 1974 1976

1974 1979 1984

26

1983-84

100 100

100

100

100

1.84

1.3

1.75 0.47-4.90 2.30 5.41 1.04 4.18 2.1 1.94 2.22 1.82 4.7 3.02 0.81 0.9 1.6 0.56 0.193 0.7 1.2 1.04 1.23

GC-ECD Focardi et at. (1986) Cantoni et at. (1986) Nishimoto et at. (1973) GC-ECD Mori et al. (1983) Fukano and Doguchi (1977) GC GC-ECD Mori et al. (1983) GLC-ECD Morita and Ohi (1975) Yoshimura (1985) Yoshimura (1985) Yoshimura (1985) Zitko (1979) GC-ECD Mori et al. (1983) GLC-ECD Solly and Shanks (1974) Zitko (1979) Zitko (1979) Juszkiewicz et at. (1977) GC Syrowatka et at. (1978) Abbott et at. (1981) GLC Zitko (1979) GLC-ECD Holt et at. (1986) GLC-ECD Holt et al. (1986) Zitko (1979) Okond' Ahoka (1984)

0

w

0\

'"0

-e' 0

0-

~

::s

3II>

~

::r:

'"Ei"

0

~

'"s.:

:;:Q

64

F.W. Kutz, P.H. Wood, and D.P. Bottimore 100 90 80

---

70

.., '" ~ ~

...... ..,__ ....

80

Dl.-n-' ....

50

40 30 20

10

1972

1973

1974

1975

1976

19n

1976

1979

1981

1983

SuMoy~y-

Fig. 7. National Human Adipose Tissue Survey (lipid adjusted): PCB residues

PCBs in ingestion (WHO 1978). Less prominent routes of human exposure are the inhalation and dermal routes. However, exposure of the general population has been primarily through the consumption of fish and shellfish (SRC 1987). Certain species of fish have been reported to accumulate PCBs to more than 100,000 times the level present in water (WHO 1978). Many published studies have reported the occurrence of PCBs in human adipose tissue. However, most of these investigators have analysed for the occurrence of total PCBs rather than quantitating individual congeners or isomers. This method of reporting is partly the result of the complex analytical techniques used to separate completely the isomers. Techniques have varied among investigators. Reported levels of PCBs in adipose tissue of the general population of various countries are presented in Table 21. Categorical data from the U.S. EPA NHA TS for fiscal years 1970-83 were used to estimate population baseline percentages that fell within various PCB residue range levels (U.S. EPA 1985b). The national baseline percentages for all fiscal years were estimated as follows: (1) 93.5% of the population had detectable levels of PCBs, (2) 66.4% had detectable levels < 1 ppm, (3) 28.9% had levels exceeding 1 ppm, and (4) 5.1% had levels exceeding 3 ppm. When the results were compared across the subpopulation, it was found that: (1) the "0-14-year" age group has a smaller percentage with detectable levels of PCBs, and a smaller percentage of individuals exceeding 1.0 ppm and 3 ppm, (2) males have a higher percentage exceeding 1 ppm than do females, and (3) the Northeast Census Region has a greater percentage of individuals exceeding 3 ppm. A time trend analysis was also performed to determine the changes in residue level distributions over time, and their difference across geographic and demographic subpopulations. Figure 7 presents the PCB analytical


65

results as the percent of population where PCB levels were: (1) not detected, (2) < 1 ppm, (3) detected between 1 and 3 ppm, and (4) > 3 ppm. This figure shows that the estimated population percentage of individuals having total PCB levels > 3 ppm has steadily declined. Table 22 presents the weighted percentage distribution of PCB residue levels in adipose tissues for each fiscal year, based on different geographic and demographic subpopulations. IX. Toxaphene Toxaphene was introduced as a new broad-spectrum contact insecticide in the mid-1940s. By 1948, it was used commercially to control a variety of insects, and for many years it was the most heavily used insecticide in the U.S. Chemically, toxaphene is described as a complex mixture of multicomponent polychlorinated camphenes. The chlorine content is estimated to be 67 to 69% (WHO 1979a). The overall composition of toxaphene approximates C1oHlOCl s . However, despite its widespread use as an insecticide for over 25 yr, its exact chemical structure is basically unknown (WHO 1979a; U.S. FDA 1981; Murphy 1986). Several research studies have indicated that technical toxaphene contains at least 177 separate components (WHO 1979a). Other estimates range from 177 to 670 components (U.S. EPA 1986a). This unusually large number of components makes it difficult to determine the presence of toxaphene in media. In the U.S., toxaphene was registered for use on a number of food and feed commodities. These commodities included mainly vegetables and fruits, cereal grains, and oilseed crops. However, the principal use of toxaphene was for cotton pests. It was also used on tobacco, sheep, swine, and cattle (U.S. FDA 1981). The use of toxaphene in the u.s. began to decline in the mid-1970s and was subsequently canceled in 1989 (Polpyk 1989). Toxaphene is believed to have been widely used in foreign countries. Reported uses include insect control on citrus, coffee, apples, sunflowers, sesame, corn, peanuts, and potatoes (U.S. FDA 1981). Toxaphene is reported to be less persistent and bioaccumulative than most organochlorine pesticides; however, because of its previous wide-spread use, significant environmental distribution has occurred. Thus, residues of toxaphene have been found in most environmental media and animals, including plants, domestic animals, and animal milk. Toxaphene has also been found in such media as fish and other aquatic organisms, nonaquatic wildlife, water and sediment, drinking water, air, soil, and food (WHO 1979a). Concentrations up to 1,750mg/m 3 have been found in the air in the cotton growing areas of Mississippi Delta (U.S. FDA 1981; WHO 1979a). Toxaphene residues were also reported in samples of cigarettes, cigars, smoking tobacco, and chewing tobacco (WHO 1979a). Previous monitoring reports, together with the pattern of extensive insecticide use, indicate that the general

6.2(1.9) 1.9 (0.6) 3.9 (1.1) 5.3 (2.0) 5.3 (2.8) 2.9 (1.2) 5.8 (2.4) 0.6(0.3) 4.0(1.1)

46.1 (5.5) 68.4(3.8) 68.2(4.1)

64.4(3.9) 58.4(4.1)

61.2(3.4) 62.8(6.2)

73.0(7.9) 51.1 (3.7) 65.8 (4.3) 53.4 (11.5)

61.4(3.4)

27.6(4.3) 31.0 (3.5)

29.5 (3.2) 27.4(6.3)

15.9 (6.1) 35.8(6.0) 28.0(5.0) 41.3 (12.4)

29.3 (3.3)

Entire nation

2.0(1.4) 5.1 (1.7) 4.8(0.9)

Percent >3 ppm"

42.2(6.6) 24.6(4.1) 22.0(3.2)

Percent (Standard Error)

Percent > 1 ppm"

Age (in years): 0-14 15-44 45+ Sex: Male Female Race: White Non-white Census region: Northeastern North central Southern Western

Subpopulation

Percent Detected But < 1 ppm"

Fiscal Year 1972

6.2 (1.3) 4.0(1.0) 4.2(0.9) 10.8 (2.8)

43.4(4.1) 27.8 (3.4) 35.4(3.4) 37.0(7.9) 46.5 (10.1) 37.0(6.6) 28.5 (3.5) 30.3 (4.8) 35.5 (3.3)

38.7 (3.9) 54.3 (4.1) 49.1 (3.6) 29.7 (7.0) 34.5 (11.2) 51.9(5.7) 47.4(4.7) 53.2(6.0) 46.5 (3.5)

Census region: Northeastern North central Southern Western Entire nation

5.1 (1.0)

6.8 (2.4) 5.0(2.3) 4.9(1.1) 3.3 (2.1)

2.1 (1.4) 4.1 (1.3) 9.2 (1.6) 11.9 (3.3) 40.5 (4.5) 51.0(4.2)

Percent >3ppm"

61.3 (6.4) 45.9 (4.3) 33.6(3.8)


Percent > 1 ppm"

Age (in years): 0-14 15-44 45+ Sex: Male Female Race: White Non-white

Subpopulation


Fiscal Year 1973

Table 22. Weighted percentage distribution of PCB residue levels in adipose tissues

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41.0(4.2) 31.5 (3.4)

35.2(3.3) 43.7 (5.0)

49.3(3.5) 59.1 (3.3)

55.5 (2.8) 46.0(7.3)

40.7(4.9) 55.0(4.8) 57.4(3.6) 66.7 (8.9)

54.3 (2.6)

Census region: Northeastern North central Southern Western

Entire nation

36.1 (3.1)

45.8 (8.2) 31.8 (5.1) 36.1 (3.4) 29.4(8.6)

8.0 (1.9) 43.9(4.5) 52.0(4.3)

72.9(6.5) 50.7(4.2) 41.7 (4.3)


Percent > 1 ppm"


Subpopulation


Fiscal Year 1974

4.6(1.2)

8.0(4.1) 3.0 (1.4) 4.9 (1.7) 2.0(1.1)

4.5 (1.3) 5.7 (2.0)

4.0(1.0) 5.2 (1.9)

0.0(--) 5.2 (1.6) 8.1 (2.5)

Percent >3ppm"

Entire nation


Subpopulation


Percent > 1 ppm"

62.0(4.0)

54.9(10.6) 62.6(6.9) 63.0(6.1) 69.4(9.0)

62.9(4.1) 56.4(6.8)

63.0(4.4) 61.1 (4.7)

71.1 (7.9) 59.5 (4.1) 57.0(5.0)

31.5 (3.1)

38.1 (7.8) 32.9(5.9) 29.8(5.1) 23.1 (5.7)

30.7 (3.0) 38.5 (6.3)

30.1 (3.7) 32.9(3.9)

9.1 (2.6) 39.0(4.1) 42.4(4.9)



Fiscal Year 1975

(Continued)

8.3 (1.5)

16.3 (3.0) 7.8 (2.9) 6.1 (3.1) 2.0(2.1)

7.7 (1.4) 12.4 (3.3)

8.7 (2.3) 7.9 (1.6)

0.5 (0.4) 8.4 (1.9) 15.4(3.6)

Percent >3 ppm"

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52.8 (3.0) 20.7(5.9) 36.1 (5.3) 30.2(8.9)

34.8 (3.1)

64.2(2.8) 60.3 (6.5)

47.4(3.0) 77.1 (6.1) 62.5 (5.4) 67.2(10.1)

63.7 (2.8)



Entire nation

34.6(3.2) 36.8(6.2)

41.9(4.1) 28.3(4.2)

56.5(4.2) 70.4(3.7)

Sex: Male Female

8.9(2.8) 43.2(3.0) 47.8(5.3)

86.6(3.4) 56.3 (2.6) 52.4(5.1)


Percent > 1 ppm a

Age (in years): 0-14 15-44 45+

Subpopulation

Percent Detected But 3 ppma

Entire nation



Age (in years): 0-14 15-44 . 45+ Sex: Male Female

Subpopulation


Percent > 1 ppm"

71.3 (2.4)

69.5 (3.4) 68.6(4.8) 75.2(5.2) 71.2(4.2)

71.5 (2.3) 69.7 (5.1)

66.7(3.4) 75.6(2.6)

90.1 (2.9) 66.8 (3.6) 59.8 (4.1)

28.1 (2.2)

29.9(3.0) 31.4(4.6) 23.5 (4.4) 28.8(4.0)

27.8(2.2) 30.9(5.1)

32.9(3.5) 23.6(2.2)

7.9(2.8) 33.2(3.6) 40.2(3.9)


Percent Detected But 3 ppm a

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32.0(3.7) 21.0(3.5)

25.8 (3.6) 30.4(4.1)

67.0(3.9) 76.4(3.6)

72.8 (3.8) 65.2(5.6)

69.4(8.9) 70.9 (5.4) 74.0(7.5) 72.8 (3.9)

71.8 (3.5)


Entire nation

26.4(3.4)

30.0(8.2) 27.1 (6.0) 24.4(7.0) 23.6(2.4)

9.2 (3.4) 31.8 (4.3) 35.0(5.1)

85.1 (4.3) 67.9 (4.4) 64.7 (5.1)


Percent > 1 ppm"


SUbpopulation


Fiscal Year 1978

8.2 (1.9)

7.4 (3.3) 7.5 (3.4) 10.6(4.3) 6.4(3.6)

8.0(2.0) 10.1 (3.4)

11. 7 (2.8) 5.0(1.5)

2.7 (1.6) 12.2(2.8) 8.0(2.5)

Percent >3ppm"

Percent > 1 ppm"

20.1 (3.8)

78.7 (3.3)

19.5 (3.8) 24.2(5.5)

22.2(3.9) 17.9(4.0)

Entire nation

79.5 (3.2) 72.7(6.1)

76.5 (3.5) 80.9 (3.5)

43.4 (11.0) 7.0(2.7) 15.9(2.7) 15.9(4.6)

6.9 (3.0) 19.7(4.7) 33.2 (5.3)

55.7 (11.7) 93.0(2.8) 81.4(4.4) 82.9(5.7)

89.0(3.5) 80.3 (4.2) 66.6(3.9)



Fiscal Year 1978


Subpopulation


(Continued)

3.9(2.5)

12.9 (10.5) 0.1 (0.1) 0.6(0.4) 3.5(2.1)

3.7 (2.5) 5.8 (2.8)

4.5 (1.9) 3.3 (3.2)

0.0(--) 4.7 (2.9) 6.6(4.3)

Percent >3 ppm" ~

0\

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III

3

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17.7 (4.3) 17.4(4.0)

15.0(3.2) 31.5 (8.9)

12.2 (2.8) 18.9 (7.2) 17.8 (7.4) 21.3 (6.8)

8203 (4.3) 82.6(4.0)

85.0(3.2) 68.5(8.9)

87.8(2.8) 81.0(7.2) 82.2(7.6) 78.7 (6.8)

82.5 (3.5)

Entire nation 0.5 (OJ)

0.0(--) 1.9 (1.2) 0.0(--) 0.0(--)

0.2(0.2) 1.9 (1.9)

1.0(0.7) 0.0(--)

0.0(--) 0.6(0.6) 0.6(0.6)

Percent >3 ppm·

Entire nation


Subpopulation

'ppm denotes part per million. (--) Standard error cannot be calculated since estimated percentage is zero.

17.5 (3.5)

12.1 (7.2) 16.1 (4.0) 23.6(4.4)

87.9(7.2) 83.9(4.0) 7603 (4.4)


Percent > 1 ppm·


Subpopulation

Percent Detected But < 1 ppm·

Fiscal Year 1981


Percent >1 ppm·

94.5 (1.7)

5.5 (1. 7)

2.4(1.8) 10.2(4.3) 4.9(2.7) 3.5 (2.4)

6.0(1.9) 1.9 (1.4)

94.0(1.9) 98.1 (1.4) 97.6 (1.8) 89.7 (403) 95.1 (2.7) 96.5(2.7)

10.9 (303) OJ (OJ)

3.1 (3.1) 3.6(2.8) 9.9(4.2)

89.1 (303) 99.7 (OJ)

96.9(3.1) 96.4(2.8) 90.1 (4.2)


Percent Detected But 3 ppm·

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71

population has been exposed to toxaphene both through inhalation and ingestion of food commodities. Knowing the concentration of a chemical within the environment is important, especially when its widespread use has occurred. However, the number of studies quantitating toxaphene levels is extremely limited. Thus, toxaphene is one of the least studied pesticides in regard to its residue levels. The main reason for this lack of research on toxaphene is the difficulty of accurately measuring toxaphene residues because of its complex chemical composition (U.S. EPA 1980b). Another difficulty stems from toxaphene's metabolism. Most, if not all, components of toxaphene are believed to undergo extensive metabolic dechlorination in mammalian systems prior to excretion. This conclusion is based on the excreted residues found in rats (U.S. FDA 1981). Metabolic dechlorination, along with the volatility and solubility differences exhibited by the complex components of insecticide, may account for the changes noted in the composition of the terminal residues when compared with the composition of the applied toxaphene (U.S. FDA 1981). Geyer et al. (1971) and Penumarthy et al. (1976) (as reported in Pollock and Kilgore 1978) have concluded that in animals, the amount of toxaphene residue that accumulates in tissues is lower than for most organochlorine pesticides, and that its elimination from tissues is rapid. A global search of the literature yielded little data on the levels of toxaphene in adipose tissue in the general population. In one study, 46 composite specimens were prepared from the NHATS repository and 14 samples representing the 45 + age category were analyzed for toxaphene. Toxaphene was qualitatively identified in 12 of the 14 samples. However, quantitation of toxaphene was not achieved because of the complexity of the response; nevertheless, it was estimated to be

Selected organochlorine pesticides and polychlorinated biphenyls in urban atmosphere of Pakistan: concentration, spatial variation and sources.

Time trends in serum organochlorine pesticides and polychlorinated biphenyls in the general population of Biscay, Spain.

Transplacental Transfer of Polychlorinated Biphenyls, Polybrominated Diphenylethers, and Organochlorine Pesticides in Ringed Seals (Pusa hispida).

Organochlorine pesticides and polychlorinated biphenyls in fish from Lake Awassa in the Ethiopian Rift Valley: human health risks.

Accumulation levels of organochlorine pesticides in human adipose tissue and blood.

Persistent organochlorine pesticides and polychlorinated biphenyls in air of the North Sea region and air-sea exchange.

Concentrations of Polychlorinated Biphenyls and Organochlorine Pesticides in Umbilical Cord Blood Serum of Newborns in Kingston, Jamaica.

Risk of female breast cancer and serum concentrations of organochlorine pesticides and polychlorinated biphenyls: a case-control study in Tunisia.

Associations of organochlorine pesticides and polychlorinated biphenyls with total, cardiovascular, and cancer mortality in elders with differing fat mass.

Levels of polycyclic aromatic hydrocarbons, polychlorinated biphenyls, and organochlorine pesticides in various tissues of white-backed vulture in India.

Polychlorinated biphenyls and selected organochlorine pesticides in serum of Slovak population from industrial and non-industrial areas.

Vertical distributions of organochlorine pesticides and polychlorinated biphenyls in an agricultural soil core from the Guanzhong Basin, China.

Residues of selected polychlorinated biphenyls (PCB) and organochlorine pesticides (OCP) in postmortem lungs from Epirus, northwestern Greece.

Organochlorine pesticides and polychlorinated biphenyls along an east-to-west gradient in subtropical North Atlantic surface water.

Organochlorine pesticides and polychlorinated biphenyls in surface soils from Ruoergai high altitude prairie, east edge of Qinghai-Tibet Plateau.

Polychlorinated biphenyls, organochlorine pesticides and chlorobenzenes content of livers from Atlantic cod (Gadus morhua) caught off Halifax Nova Scotia.

Organochlorine compounds in human adipose tissue from north Texas.

Abundance and distribution of polychlorinated biphenyls (PCBs) in breast tissue.

Polychlorinated biphenyls and organochlorine pesticides in surface sediments from the sand flats of Shuangtaizi Estuary, China: levels, distribution, and possible sources.

Levels of polychlorinated biphenyls, organochlorine pesticides, and chlorophenols in the Kupa River water and in drinking waters from different areas in Croatia.

[Residue analysis of chlorinated pesticides and polychlorinated biphenyls (PCB) in fish and waters 2 (author's transl)].

Estimation of measurement uncertainty of polychlorinated biphenyls, polycyclic aromatic hydrocarbons and organochlorine pesticides in the atmosphere using gas chromatography-mass spectrometry and gas chromatography-electron capture detector.

Organochlorine pesticides and polychlorinated biphenyls in grass, yak muscle, liver, and milk in Ruoergai high altitude prairie, the eastern edge of Qinghai-Tibet Plateau.

Occurrence of brominated flame retardants (BFRs), organochlorine pesticides (OCPs), and polychlorinated biphenyls (PCBs) in agricultural soils in a BFR-manufacturing region of North China.