Showing papers in "Environmental Health Perspectives in 1973"

Toxicology of chlorinated dibenzo-p-dioxins.

Abstract: Severe toxicological responses have been associated with certain chlorodibenzodioxins. One of these responses is chloracne, a folliculosis first associated with skin contamination by chlorohydrocarbons in 1899 (1)). Serious outbreaks of chloracne-like lesions associated with runaway reactions in the production of 2,4,5-trichlorophenol occurred in Germany in the early 1950's (2). 2,4,5Trichlorophenol itself does not cause acne (3), but the contaminants which may be formed in the uncontrolled production of 2,4,5-trichlorophenol are extremely potent acnegens (2). 2,3,7,8-Tetrachlorodibenzo-pdioxin and triand tetrachlorodibenzofuran were isolated from the contaminants formed in 2,4,5-trichlorophenol production and were demonstrated to be strongly positive acnegens when applied to rabbit ears (3). By using the rabbit ear test, the acnegenic potency of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) was confirmed in 1962 (4). In addition, 2,3,7,8-TCDD is extremely toxic in the chick embryo assay (5) and is highly embryotoxic in rats (6). Another chlorodibenzodioxin, hexachlorodibenzo-pdioxin (HCDD), is known to be positive for the chick edema factor, a condition characterized by hydropericardium, ascites, and anasarca (5, 7).

Toxicity and health threats of phthalate esters: review of the literature.

Abstract: poly(vinyl chloride) (PVC) plasticized with EDHadEven thoug ther reports had implied that certain formulations of PVC medical tubings (2,3) and containers would, in fact, release plasticizers as well as additives to solutions, little concern had been expressed as to the possible health consequences to humans from leaching of these agents. Since Jaeger and Rubin's publication, however, considerable interest has developed conceming the possible toxicogenic effects not only of DEHP, but of all hthalate esters. More recently, interest has lso cen O the potential hazards from these plasticizers in the environment. It is estimated that the

Organotin compounds: industrial applications and biological investigation.

Abstract: According to Ross (1), there are three main areas in which organotin compounds have product and process utility: (1) heat stabilizers; (2) catalytic agents; (3) biocidal compounds. Organotin derivatives account for the fourth largest production of organometallics amounting to about 3-4 million pounds per year as compared with about 485 million pounds per year for organolead compounds. Originally, organotin compounds were developed as thermal stabilizers for chlorinated hydrocarbons which would be used in those applications for which there was a strong possibility of thermal degradation. However, as the chemistry of organotin compounds became better understood, their application expanded to catalytic and biologically active agents.

Pathologic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in laboratory animals.

Abstract: ImagesFIGURE 1.FIGURE 2.FIGURE 3.FIGURE 4.FIGURE 5.FIGURE 6.FIGURE 7.FIGURE 8.FIGURE 9.FIGURE 10.FIGURE 11.FIGURE 12.FIGURE 13. AFIGURE 13. B

Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin on the immune system of laboratory animals.

Abstract: ImagesFIGURE 1.FIGURE 2.FIGURE 3. aFIGURE 3. bFIGURE 4.FIGURE 5.

Phthalate ester plasticizers--why and how they are used.

Abstract: Phthalate esters have been found in the environment. They have also been detected in humans and animals. We do not know how they enter the environment nor do we know if they present a hazard to mankind. Strong evidence exists pointing to the natural occurrence of the phthalate moiety. However, we do not know to what extent these natural sources contribute to the total amount found in the environment. This meeting of industrial, academic, medical, and government scientists from many disciplines will give the public, whom we all serve, a better understanding of these issues than if we individually pursued our separate courses. The public deserves the best scientific opinions we can give them opinions based on meaningful research and interpreted with unemotional perspective. The objective of this presentation is to provide specific aspects of plasticizer technology and market data necessary for environmentalists and toxicologists to understand the possible points of entry of these phthalate esters into the environment or the human body: the esterification process; ester transport; polymer-plasticizer process; enduses; disposal; natural sources. Only a small portion of the storehouse of plasticizer technology can be reported here. Phthalates are used in virtually every major

An analytical method for detecting TCDD (dioxin): levels of TCDD in samples from Vietnam.

Abstract: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an extraordinarily toxic substance that is produced as an unwanted side product in the industrial synthesis of 2,4,5-trichlorophenol, an intermediate in the manufacture of the herbicide 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) (1, 2). Because of its chemical stability and its lipophilic nature, the possibility exists that TCDD released into the environment could accumulate in food chains. A direct test of the possibility of biologically significant accumulation in animal tissues requires an analytical method able to detect TCDD at levels well below those known to be toxic. The lowest value known for the lethal dose of TCDD is that observed in the guinea pig, for which the single oral dose LD50 is 600 parts per trillion (ppt) body weight (3). Allowing for sublethal toxic effects and providing for a conservative margin of safety, it seems desirable to have an analytical sensitivity of at least 1 ppt. For a 1-g sample this means the method must have a sensitivity of, about 10-'2g or 1 picogram (pg). The most common method for analyzing chlorinated organic compounds in tissue samples is gas-liquid chromatography (GLC) with an electron capture detector. Its limit

General biological effects of TCDD in laboratory animals.

Abstract: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is reported to be one of the most toxic chemicals known. There has been variation in such reported toxic parameters as single oral LD50 dose, range of time interval from dosing until death, and toxic manifestations which an animal exhibits (1-4). It seemed most appropriate, therefore, that the mean values and ranges of these and other general biological parameters be determined under the experimental condition to which animals are exposed at this Institute.

Toxicity of metabolites produced by the "Alternaria"

Abstract: The presence of toxin-producing fungi in foodstuffs and other agricultural commodities is well established (1-3). The Alternaria, Aspergilli, Fusaria and Penicillia have been repeatedly implicated as the principal coinhabitants of products in which toxicity has been demonstrated (4,5). Numerous compounds have been isolated that can explain the toxicity of the Aspergilli, Fusaria, and Penicillia. Among the more important of these are the aflatoxins, patulin, penicillic acid, and sterigmatocystin, because of their carcinogenic potential; the ochratoxins, citrinin, cyclopiazonic acid, and the estrogenic zearalenone because of a variety of high toxicities and their frequent appearance in moldy foodstuffs. By comparison, toxic components of the Alternaria have been studied to only a small extent. The Alternaria are found on wheat, barley, oats, sorghum, corn, and peanuts (4,6,7). Animal feeds and silage that contain these crops, as well as alfalfa and grass hay are also good sources (4). The Alternaria are plant pathogens and thus can contaminate food through field infection as well as through storage. Black spot of Japanese pear, brown

A survey of the embryotoxic effects of TCDD in mammalian species.

Abstract: on the embryotoxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). This is true for the number of animals used per experimental group, especially in the higher dose range, as well as for the number of dif

Excretion and tissue distribution of 2,3,7,8-tetrachlorodibenzo-p-dioxin in the rat.

Abstract: The compound, 2,3,7,8-tetrachlorodibenzop-dioxin (TCDD), is highly toxic. The LD50 for male and female rats given a single oral dose is 23 and 45 pg/kg, respectively (1). Adverse effects have been observed in a teratology study in which pregnant rats were given oral doses of 0.125-2.0 pg/kg-day TCDD from day 6 through day 15 of gestation (2). The adverse effects were increased fetal mortality, early and late resorptions and intestinal hemorrhage in the fetuses. No adverse effects were noted at the 0.03 ptg/kgday level. In humans and rabbits, contamination of the skin with TCDD produces chloracnelike lesions (3, 4)1. This disease is characterized by the appearance of hyperkeratosis, papules, comedones and cysts. There is no available information on the absorption, excretion or tissue distribution of TCDD in animals. Therefore, this study was done to determine the excretion and tissue distribution of radioactivity derived from TCDD-14C following a single oral dose of the labeled compound.

Etiology of chick edema disease.

Abstract: Chick edema disease first came to the attention of the Food and Drug Administration in December, 1957, when it was learned that millions of broilers died in the eastern and Midwestern parts of the United States. Several groups in industry and government quickly determined that the disease was due to toxic components in certain feed fats (1-3), and that toxicity was associated with the unsaponifiable portion of the fat. Characteristic symptoms included the presence of excessive fluid in the heart sac and in the abdominal cavity of chicks fed toxic fat (2, 4, 5). These and other symptoms such as subcutaneous edema and liver necrosis were accompanied by high mortality beginning approximately in the third week. Allen (6, 7) suggested several years later that the accumulation of large quantities of extravascular fluid in chickens might be due to altered permeability of the vascular bed as well as cardiac decompensation and liver necrosis.

Postnatal effects of maternal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

Abstract: ImagesFIGURE 1.FIGURE 2.

Model ecosystem studies of the environmental fate of six organochlorine pesticides.

Abstract: Despite more than 20 years of intensive use there are major uncertainties about the environmental distribution and degradative fate of the various organochlorine pesticides in food web organisms. The problem is both controversial and momentous, as 88,641,000 pounds of cyclodienes and toxaphene and 59,316,000 pounds of DDT were produced in the United States in 1970 (1). The laboratory model ecosystem devised in this laboratory (2) has been used to estimate the comparative environmental properties of DDT, methoxychlor, and other DDT analogs (3-5). These investigations have demonstrated environmental degradative pathways and have provided quantitative data on ecological magnification and biodegradability index (6). This paper presents data on six additional organochlorine pesticides which should be of value in judging their overall effects on environmental quality. Furthermore, the data provide a realistic background of the environmental toxicology of standard substances against which screening data for new candidate pesticides can be weighed.

TCDD-induced changes in rat liver microsomal enzymes.

Abstract: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a contaminant of the herbicide 2,4,5trichlorophenoxyacetic acid (2,4,5-T), is extremely toxic (1), although the mechanism of toxicity is not known. Other papers presented at this conference cover the spectrum of environmental and health hazards of chlorinated dibenzodioxins and dibenzofurans. It should suffice to say here that these compounds are teratogens (2-4) in rodents, and the extensive use of 2,4,5-T, especially in Vietnam, has focused concern on their potential health hazards. Recently TCDD was shown to be an inducer of 8-aminolevulinic acid synthetase in the chick embryo (5) and also to decrease hexobarbital sleeping times in rats (6). These reports prompted us to investigate the effects of sublethal doses of TCDD on activities of hepatic microsomal and mitochondrial enzymes. The microsomal enzymes include components that are involved in the detoxication of foreign compounds and the regulation of many endogenous compounds such as the steroid hormones (7). Microsomal constituents and activities investigated in this study were: cytochrome P-450, cytochrome b5,

Hematologic and clinical chemistry effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in laboratory animals.

Abstract: Chlorodibenzo-p-dioxins, especially 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD), are among the most toxic compounds known. These compounds are found as contaminants of technical chlorophenols and their derivatives. A variety of pathologic condition have been associated with the ingestion of products containing chlorodibenzo-p-dioxins. Toxic fat, the cause of chick edema disease (1, 2) and a variety of pathologic manifestations in monkeys (3), has been found to contain chlor3dibenzo-p-dioxins, among which is TCDD (4, 5). TCDD has been implicated in a variety of other toxicoses, including outbreaks of chloracne in chemical workers (6), hepatonecrosis in rabbits (6), and hepatonecrosis and thymic atrophy in rats (7). However, only in the studies in which monkeys were fed toxic fat (3) and in which rats were given TCDD orally (7, 8) were substantial clinical pathologic analyses performed. Toxic fat caused in the monkeys, among other lesions, anemia, leukopenia and hypoproteinemia. The hypoproteinemia was primarily due to decreased serum albumin concentration. The blood urea nitrogen

Some general principles of mutagenicity screening and a possible framework for testing procedures.

Abstract: It is likely that the assessment of chemicals for mutagenicity will soon become a widespread practice, and a large number of different screening procedures have been proposed The subjection of every new chemical to be released into the environment to every available test is clearly an impossible task, and it is necessary for an understanding of priorities in terms of risk and benefit to be built into any approach The present paper represents an attempt to frame a protocol for the assessment of new compounds that is concerned not with the details of individual tests but rather with the questions these tests should be designed to answer and to the evaluation of the answers obtained It is obviously inherent in such an approach that a similar assessment must be made of chemicals already in the environment, but that is not the purpose of the present article Genetic hazards (with the exception of nondisjunction and some other chromosomal abnormalities) are very different from toxic hazards, in that there is little or no likelihood of any feedback from human epidemiological data Toxicologists have stressed (1) that, despite all the animal testing of the past two decades and before, most of what we know about toxic hazards

Studies on the bioaccumulation and microbial degradation of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Abstract: While the problem of pesticidal contamination of the environment is far from being solved, considerable useful information has emerged from the research efforts made by many scientists in recent years. First, we now know by experience that the chemicals that cause environmental problems are the ones which are extremely persistent in nature, biologically active, and easily concentrated in biological systems. Compounds which lack any of the above qualifications usually do not play any significant role in pesticidal pollution no matter how acutely toxic they are. The above analysis becomes more important, when one considers other aspects of pesticidal pollution. For instance, we are concerned about only biological effects in considering pollution, with particular emphasis on the effects on nontarget organisms. In the case of polychlorinated dibenzo-pdioxins, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the question of bioactivity is indisputable, as it is one of the most toxic compounds known to occur as a pesticidal impurity (1-3). Its chemical stability is also questionable. Thus the central question of its hazard to the environment must be stud-

Toxicology of phthalic acid esters in aquatic organisms.

Abstract: Phthalic acid esters are presently being used in amounts and products that can easily, although inadvertently, contribute to environmental pollution. As plasticizers, phthalic acid esters are added to synthetic plastic resins to impart flexibility to the finished product, improve workability during fabrication, and extend or modify properties not present in the original resins (1). Plastic formulations may contain up to 60% of plasticizers (2). Phthalic acid esters are the most widely used plasticizers, particularly in poly(vinyl chloride) plastics. More than 800 million pounds of these plasticizers were produced in 1969 (1). Di-n-butyl and di-2ethylhexyl phthalates are used as plasticizers and also as an insect repellant and orchard acaricide, respectively (3). Phthalic acid esters have been identified as environmental contaminants because of their discovery in soil (4), a deep sea jellyfish (5), aquatic organisms and water (6), and bovine tissues (7,8). The acute toxicities of various phthalic acid esters have been determined in mammals and birds and the compounds were found to have a very low order of toxicity (3,9-12). Teratogenic effects of phthalic acid esters have been demonstrated in rats (13). Problems of phthalic acid esters leaching from plastics used in human medical practices have also been reported (14-17). The biological significance of phthalic acid ester residues in aquatic organisms is un-

Determination of chlorinated dibenzo-p-dioxins and dibenzofurans in various materials.

Abstract: The determination of specific chlorinated dibenzo-p-dioxins is complicated by the large number of structurally similar compounds which are normally present in many samples as well as the usual problems of removal of the matrix itself. Thus separation techniques with the highest resolving power and detectors with the most specific response must be used. The certainty of the results must be established so that proper action can be taken to prevent exposure by plant personnel and to assure that these materials are not spread in the environment. In order properly to assess the wide range of biological activity which these compounds exhibit, the final determination must be specific, sensitive, and reliable. The search for such a method began at Dow Chemical Company in 1964 when the caustic insoluble residue from 2,4,5-trichlorophenol distillation residue was examined by thin-layer chromatography and the most biologically active spot identified as 2,3,7,8tetrachlorodibenzo-p-dioxin by comparison with synthesized material (N. E. Skelly, Dow Chemical Company, personal communication, 1964). The isolated and synthesized materials were compared and examined by mass spectrometry, infrared spectrometry,

Uptake and fate of Di-2-ethylhexyl phthalate in aquatic organisms and in a model ecosystem.

Abstract: Di-2-ethylhexyl phthalate (DEHP), often referred to as dioctyl phthalate or DOP, is the most widely used plasticizer for vinyl plastics, and approximately 350 million pounds were produced in the United States during 1970. Altogether the production of phthalate ester plasticizers was 855 million pounds (1). The cumulative production of DEHP and related phthalate plasticizers in the United States since 1943 is in excess of 8000 million pounds (2). DEPH is an external plasticizer which softens resins without reacting with them chemically, and it may be present in concentrations up to 40% of the weight of the plastic as in the familiar laboratory tubing. As a result of the large production and wide distribution and destruction of plastics, DEHP has become uniquitous and has been found in milk (3), deep frying fat (4), and human blood plasma (5). DEHP has also begun to appear as a micropollutant in the tissues of a variety of organisms. Taborsky (6) isolated it from bovine pineal glands, and Nazir et al. (7) found it in mitochondria from the hearts of cattle, dogs, rabbit, and rat. DEHP has been

Some pharmacologic and toxicologic effects of di-2-ethylhexyl phthalate (DEHP) and other plasticizers.

Abstract: With the recent demonstration of the migration of phthalate ester plasticizers from vinyl plastic biomedical devices (1-4), its identification in human and animal tissues (5, 6), and evidence for its ubiquitous distribution in the environment (7, 8),tt it has become necessary to reevaluate the toxicologic potential of this class of chemical compounds. Di-2-ethylhexyl phthalate (DEHP), as an example of the most widely used of the phthalate esters, deserves particular emphasis. In general, the phthalate esters have been reported to have a low order of acute toxicity (9-11). For example, of eight different phthalate esters examined in one study, the intraperitoneal LD50 dose in mice ranged from 1.5 to 14.2 g/kg. In rats, the intraperitoneal LD50 of DEHP has been reported by several investigators to range from 2 to 31 g/kg. One report

Teratogenicity, mutagenicity, and cellular toxicity of phthalate esters.

Abstract: Growing concern that phthalic acid esters (PAE) may present a health hazard and possible deleterious effects on the ecological system has led to increased interest in the more subtle toxicity of those compounds. Although the acute toxicity of PAEs as a group is quite low, the intrinsic cellular toxicity increases with molecular weight. Whether the intrinsic toxicity is great enough to exert a significant effect in vivo at the typically low levels of solubility of PAEs is of primary importance to the assessment of their potential hazard. This paper reviews work reported on the teratogenicity of PAEs and new work on the mutagenicity, cellular toxicity, and absorption, excretion, and distribution of those compounds. The relationship of in vitro and in vivo response is discussed.

Extraction, localization, and metabolism of di-2-ethylhexyl phthalate from PVC plastic medical devices.

Abstract: The results of our studies on the extraction and disposition of three plasticizing substances which are extracted from polyvinyl chloride) medical devices will be reported. The plasticizers are di-2-ethylhexyl phthalate (DEHP), di-2-ethylhexyl adipate (DEHA), and butylglycolyl butyl phthalate (BGBP). DEHP extraction will be described in greater detail, and the two other plasticizers, DEHA and BGBP, will only be mentioned briefly. The compound DEHP is an aromatic diacid ester that meets the physical criteria needed to soften and plasticize the rigid polymer polyvinyl chloride) (PVC). As a

Phthalate ester residues--their metabolism and analysis in fish.

Abstract: During the course of our analysis of fish and other aquatic materials for pesticide residues, unknown components were often detected. Concern about the identity of late eluting gas-liquid chromatographic (GLC) peaks in fish and water extracts led to the identification of phthalic acid esters (PAEs) as environmental contaminants (1). Further study of these contaminants with a GLC-mass spectrometer (GLC-MS) led to their identification as di-2-ethylhexyl phthalate (DEHP) and di-n-butyl phthalate (DBP). Preliminary data from acute toxicity tests indicate that these compounds are relatively low in toxicity. Chronic studies, however, indicate that they may have more subtle effects on reproduction of some aquatic species (2). Residue data obtained from a variety of areas, dietary materials, and samples related to fish rearing operations have established some information on the incidence of PAEs in relation to pesticides and polychlorinated biphenyl contaminants (Table 1). PAE residues in water appeared to be correlated with rivers draining industrialized or heavily populated areas (John Hesse, Michigan Department of Natural Resources, East Lansing, Michigan 1972 personal communication). However, the distribution of PAEs in the aquatic environment remains to be defined. PAEs are commonly used as plasticizers, especially in poly(vinyl chloride) plastics. In

Carcinogens are mutagens: their detection and classification.

Abstract: We detect mutagens by using a special set of bacterial tester strains We have described our test system for mutagen and carcinogen detection in a series of recent papers I will give here only a summary of some of these results, omitting references to other work, which is credited in our original papers A simple procedure for combining human (or rat) liver for carcinogen activation and the bacteria for detection and classification is used We show that a wide variety of carcinogens (aflatoxin, benzpyrene, acetylaminofluorene, etc) are frame shift mutagens after activation and can be detected with these strains We explain the structure of these carcinogens on the basis of the theory of frameshift mutagenesis We postulate that carcinogens cause cancer by somatic mutation and suggest what the combined bacteria/ liver system be used as a simple procedure for carcinogen detection

Distribution, metabolism, and excretion of di-2-ethylhexyl phthalate in the rat.

Abstract: It has become increasingly evident in recent years that the dialkyl phthalate esters are widely distributed in our environment (1-4). As an explanation of this wide distribution there are many possible pathways by which these chemicals can be introduced into the human body. Jaeger and Rubin (5) have shown that di-2-ethylhexyl phthalate (DEHP) can be found in the tissues of patients who have received transfusions of blood stored in plastic bags. Moreover, the possibility of introducing significant quantities of phthalate esters to the system through ingestion of foodstuffs contaminated with these materials cannot be ignored. In order more fully to understand the toxicological implications of phthalate ester contamination, it is important to determine the fate of these materials once they are within the body. The study described here was undertaken in order to ascertain the distribution, metabolism, and elimination of DEHP administered to rats.

Effect of phthalate esters on reproduction in rats.

Abstract: Numerous plastic devices and materials used for medical, dental, and food collection, processing, and packaging are made of polyvinyl chloride) and plasticized mainly with di-2-ethylhexyl phthalate (DEHP) to impart the desired physical and chemical characteristics. Some finished products may contain more than 40% plasticizer, which may be leached from the material by blood (1) or milk (2) or various other solutions. DEHP has generally not been considered to be a health hazard because of its low acute oral toxicity (3-10) and because the amount of DEHP leached from plastics is quite small. However, there is evidence that DEHP is not readily hydrolyzed but accumulates in body tissues. When two patients were infused with blood stored in plastic blood bags plasticized with DEHP, Jaeger and Rubin (11) found DEHP in the spleen, liver, lung, and abdominal fat in concentrations ranging from 2.5 to 27 mg-% (dry weight). The teratogenic effects of several phthalate esters when injected into the yolk sac or allantoic cavity or applied to the chorioallantoic membrane of developing chick embryos have been reported by Haberman and others (12-14). More recently, tDepartment of Dairy Science, Michigan State University, East Lansing, Michigan 48823. *To whom reprint requests should be sent. *Supported by the Michigan Agricultural Experiment Station (journal article 6113). Singh et al. (15) have reported the teratogenicity of phthalate esters in rats without regard to the effect these compounds might have on parturition. The present study was undertaken to determine the effects of dibutyl phthalate, dimethyl phthalate, and di-2-ethylhexyl phthalate on embryonic development and parturition.

Studies on the mechanism of toxicity of the chlorinated dibenzo-p-dioxins.

Abstract: Concern about the potential health hazards resulting from environmental pollution by the chlorinated dibenzo-p-dioxins and dibenzofurans arises from our recognition of the extraordinary potency of these compounds as toxins and teratogens and their inadvertent dispersion in the environment as contaminants of chlorinated phenolic products. Questions concerning the extent of environment contamination and those concerning the mechanism of toxicity produced by these compounds are at present unanswerable. Several papers in this symposium have presented the historical background which led to our current understanding and concern about this problem: (1) the "chick-edema" outbreaks caused by "toxic fats" in poultry feed and the eventual isolation and identification of a hexachlorinated dibenzo-p-dioxin; (2) the occurrence of acne among workers in several 2,4,5-T factories and recognition of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as the etiologic agent; (3) the NCIcommissioned study on the potential teratogenicity, carcinogenicity and mutagenicity of 2,4,5-T; (4) and the widespread use of Agent

Biological responses of the nonhuman primate, chicken, and rat to chlorinated dibenzo-p-dioxin ingestion.

Abstract: ImagesFIGURE 1.FIGURE 2.FIGURE 3.FIGURE 4.FIGURE 5. aFIGURE 5. bFIGURE 6.FIGURE 7.FIGURE 8.FIGURE 9.FIGURE 10.