Elevated dioxin blood levels in British chemical workers.
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Chemical Industry↗
Biomedical subjects
A Schecter
Publications and source records attributed to A Schecter.
Congener-specific levels of dioxins and dibenzofurans in U.S. food and estimated daily dioxin toxic equivalent intake.
Food, especially meat, milk, and fish, is the immediate source of almost all polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and dioxinlike compounds in the general population. To estimate intake of these highly toxic compounds, we performed congener-specific dioxin analyses for the first time on U.S. food for 18 dairy meat, and fish samples from a supermarket in upstate New York. 2,3,7,8 Tetrachlorodibenzo-p-dioxin (TCDD, "dioxin") toxic equivalents (TEqs) on a wet weight basis for the dairy products ranged for 0.04 to 0.7 ppt, meat TEqs ranged from 0.03 to 1.5 ppt, and fish TEqs ranged from 0.02 to 0.13 ppt. Previous human breast milk and infant formula analyses were used with the current preliminary food data to estimate a range of dioxin intake for Americans. Average daily food intake of TEqs for an adult weighing 65 kg was estimated to be between 0.3 and 3.0 pg/kg body weight, for a total of 18-192 pg TEq, using 1986 American consumption rates. Due to the relatively high level of PCDDs and PCDFs commonly found in human breast milk from American women and from women in other industrial countries, a nursing infant may consume an average of 35-53 pg TEq/kg body weight/day in its first year of life. This may be compared with the current U.S. EPA virtually safe dose of 0.006 pg TCDD/kg body weight per day over a 70-year lifetime based on an upper limit cancer risk of 10(-6), or the 10 pg/kg/day used by some European government agencies.
Adult↗
Chlorinated and brominated dioxins and dibenzofurans in human tissue following exposure.
With substantial improvements in analytic techniques over the past decade, it has become possible to measure polychlorinated dioxins (PCDDs) and dibenzofurans (PCDFs) in human tissue in a congener-specific fashion down to the low parts per trillion level. This paper reviews findings using these new techniques from a number of recent medical and environmental case studies. These studies include those of workers exposed to a polychlorinated biphenyl (PCB) transformer fire in the United States, German chemical workers exposed to 2,3,7,8-tetrachlorodibenzodioxin (2,3,7,8-TCDD) while cleaning up after an explosion, workers at a municipal incinerator in New York City, a chemist exposed to brominated and chlorinated dioxins, U.S. veterans and also Vietnamese civilians exposed to Agent Orange contaminated with TCDD in Vietnam, and victims of the polychlorinated dibenzofuran and PCB contaminated rice oil (Yusho) incident in Japan.
Adipose Tissue↗
Polychlorinated biphenyl levels in the tissues of exposed and nonexposed humans.
Polychlorinated biphenyls (PCBs) are synthetic chemicals, manufactured in volume from about 1929 to the 1970s. Environmental contamination by PCBs has been documented in various substances, including human tissue. PCBs have been measured in human tissue by a variety of analytical methods. PCB levels have been reported as an approximation of total PCB content expressed in terms of a commercial mixture, by identification and quantification of chromatographic peaks, or by qualitative and quantitative characterization of specific congeners. Until recently, the coplanar mono-ortho- and di-ortho substituted PCBs, which are especially toxic and present in significant concentration in humans from industrial countries, had not been measured in human tissues. Examples of various types of commonly used analyses are presented in general population subjects and in persons who experienced special exposure. In this paper, the usefulness of PCB blood determinations following potential exposure is demonstrated, and their application in health studies is illustrated from a number of case studies. Coplanar PCB, mono-ortho-substituted and di-ortho-substituted PCB levels in human blood are presented and compared with polychlorinated dioxin (PCDD) and polychlorinated dibenzofuran (PCDF) levels in the U.S. population. Dioxin toxic equivalents for the two groups of chemicals are calculated and compared. It is found that mono-ortho-substituted and, to a lesser extent, coplanar PCBs, contribute substantially to dioxin toxic equivalents (TEq) in blood from U.S. adults. Because of substantial PCB contribution to dioxin toxic equivalents, total dioxinlike toxicity can only be determined if dioxins, dibenzofurans, and dioxinlike PCBs are measured.(ABSTRACT TRUNCATED AT 400 WORDS)
2,4,5-Trichlorophenoxyacetic Acid↗
Chlorinated dioxins and dibenzofurans in human tissue from general populations: a selective review.
During the past decade a considerable amount of data has been generated concerning polychlorinated dibenzodioxin (PCDD) and polychlorinated dibenzofuran (PCDF) levels in humans from many geographical locations. To organize these data in a useful fashion for environmental purposes and for consideration of human toxicity, selected portions of our data are presented in a somewhat atypical fashion, by percentage contribution of individual congeners to total PCDD/Fs in human tissue, and to the total dioxin equivalents (TEq). This is done to better characterize congener contributions from environmental contamination in various geographical regions at this time and health-related levels. To present the findings in a global perspective, data from widely different locations are presented including the United States, Germany, Vietnam, the former Soviet Union, Thailand, Cambodia, China, South Africa, and Guam.
Adipose Tissue↗
Use of PCB blood levels to assess potential exposure following an electrical transformer explosion.
Following the explosion of a transformer, passersby, building occupants, and cleanup personnel had potential exposure to the transformer dielectric fluid containing polychlorinated biphenyls (PCBs). As part of a medical evaluation, blood serum was analyzed for PCBs, and the concentrations found were similar to that of a regional comparison group (median 4.0 ng/mL or parts per billion, range 1-10, n = 60). Some workers employed by the utility company that owned the transformer had potential exposure to PCBs in the past. This positive comparison group had significantly higher serum PCB concentrations, related to known direct contact (median 5.0, mean 14 ng/mL, 1-187, n = 25) or not (median 4.0, mean 11 ng/mL, 2-72, n = 17). Therefore, in this investigation, elevation of serum PCB levels could be related to past contact during work with transformers, but not to potential short-term exposure at the time of a transfer explosion.
Aroclors↗
Persistent brominated and chlorinated dioxin blood levels in a chemist. 35 years after dioxin exposure.
This is the first report on occupational health hazards to dioxin chemists associated with laboratory exposure to 2,3,7,8-tetrabromodibenzodioxin (TBrDD), and further characterizes the human response to 2,3,7,8 tetrachlorodibenzodioxin (TCDD). In this case study the chemist was exposed on two separate occasions. In March 1956, after synthesizing 10 g of TBrDD, the chemist suffered from mild and transient chloracne of the neck and wrists; in September 1956, after synthesizing 16 g of TCDD, he suffered severe chloracne of the entire body, headaches, backache, and leg pain on exertion. His measured 2,3,7,8-TBrDD in 1991 was 625 parts per trillion (ppt) in whole blood lipid, 35 years after initial exposure and 18 ppt TCDD, an elevated level in comparison with the mean 2,3,7,8-TCDD level of 5 ppt in the US population. This is the first reported detection of a brominated dioxin in human tissue. The total halogenated dioxin body burden in September 1956 is estimated to have been between 13,005 ppt and 146,726 ppt. This amount can be considered to be, at least in this person, a strong chloracnegenic dose, and a dose causing human nervous system and muscular or circulatory system responses. This uptake demonstrates an occupational hazard to chemists and chemical workers, and the usefulness of human tissue dioxin measurements to document absorption.
Adult↗
Accidental exposure of children to polychlorinated biphenyls.
Children exposed to polychlorinated biphenyls (PCBs) while playing with parts of a capacitor had elevated serum concentrations of lower chlorinated PCBs, similar to Arochlor 1242. These levels declined over 11 months of followup to about half their initial values, from a mean of 12.9 to 6.3 ppb (parts per billion, ng/mL) among four children. In comparison, other persons in the same household and a reference group of persons seen in the same geographic area had serum levels of Aroclor 1242-like PCBs below the limit of detection (less than 5 ppb). All three groups--the children, household members, and geographic referents--also had higher chlorinated PCBs in their serum similar to Aroclor 1260 (HPCBs). HPCB concentrations were similar in these groups (approximately 2 ppb) and did not decline significantly.
Accidents↗
Dioxin levels in adipose tissues of hospitalized women living in the south of Vietnam in 1984-89 with a brief review of their clinical histories.
Agent Orange, a phenoxyherbicide consisting of 50% 2,4-D and 50% 2,4,5-T, the latter contaminated in the parts per million range with the highly toxic dioxin, 2,3,7,8-TCDD, was sprayed in the south of Vietnam from 1962 to 1971. The chemicals are of concern because of their potential to be causally involved in cancer, adverse reproductive outcomes, immune deficiency and other illness. Because exposed women would be especially involved in the adverse reproductive outcomes, specifically spontaneous abortions and congenital malformations, as well as developmental deficiencies in children, we elected to conduct a pilot study in Vietnam to determine whether elevated 2,3,7,8-tetrachloro-p-dioxin-(TCDD), the dioxin characteristic of Agent Orange could still be found in some women between one and two decades after exposure, and whether the types of illness characteristic of dioxins was present in women with elevated dioxin levels. We were easily able to find some women with increased TCDD from Agent Orange, A surprisingly high level of dioxins from industrial sources was also found in these women in the south. Much lower levels of all dioxins were found in patients in the north of Vietnam. No obvious relation between elevated dioxins and disease was noted in this pilot study, which is meant to precede epidemiology studies which will test the hypotheses that elevated dioxins in humans may lead to an increase in adverse reproductive outcomes and in rates of certain cancers.
Adipose Tissue↗
Toxicity and evidence for metabolic alterations in 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated guinea pigs fed by total parenteral nutrition.
The effect of total parenteral nutrition (TPN) on the toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in male, Hartley-strain guinea pigs was determined. At a single dose of 2 micrograms TCDD/kg, TPN-fed guinea pigs maintained body weight at a level which was slightly, but consistently, below that of the TPN-fed control animals. However, despite the sustenance of body weight, TCDD-treated animals died or were sacrificed due to morbidity between Days 8 and 24 following treatment. Approximately 50% of this group demonstrated a profound loss of body weight within a few days prior to death or sacrifice. With the exception of the pattern of weight loss, the signs of toxicity in the TPN-fed, TCDD-treated animals were strikingly similar to those observed in TCDD-treated guinea pigs fed ad libitum. Although livers from TCDD-treated, TPN-fed animals demonstrated increased content of lipid and cytochrome P-450, this tissue appeared to be morphologically and functionally comparable to that from TPN-fed controls. Of the blood chemistry examined, only the serum concentrations of 3,5,3'-triiodothyronine were significantly decreased in the treated animals fed by TPN. Results were also compared to TCDD-treated guinea pigs fed ad libitum and respective pair-fed controls. Many of the physiological and biochemical responses observed in animals fed ad libitum following TCDD treatment could be explained by a decrease in food consumption. This study demonstrated that although food consumption clearly accounts for the major effect of TCDD on body weight loss in guinea pigs fed ad libitum, additional physiological and/or biochemical alterations occurred which also contribute to body weight loss, other signs of toxicity, and subsequent lethality.
Animals↗
Growth and hepatic composition in the guinea pig after long-term parenteral hyperalimentation.
This study examined the feasibility of maintaining male Hartley guinea pigs on long-term hyperalimentation. Data from animals fed ad libitum, but infused with 0.9% saline, indicated that there was minimal effect from catheter implantation, sepsis, or the infusion of large volumes of fluid. This group compared with animals fed and watered ad libitum demonstrated a nearly identical growth rate (6.33 +/- 1.18 and 6.12 +/- 1.32 g/day, respectively), serum chemistry, tissue weights, and hepatic composition and morphology. Animals infused with a total parenteral diet demonstrated growth rates of 4.06 +/- 1.46 g/day for up to 25 days. Loss of infused animals was due in varying degrees to sepsis, mechanical failure, improper placement of the cannula, loss of patency, and death from unknown causes. Morphological analysis of animals fed by total parenteral nutrition revealed an altered distribution and increased size of lipid droplets in hepatic parenchymal and Kupffer cells and glycogen accumulation by the parenchymal cells. Decreased hepatic content of total protein and lipid, as well as cytochrome P450, was also observed. Similarly, serum values of triglyceride were decreased in animals fed by the total parenteral diet. This study indicated that the guinea pig fed by hyperalimentation may be a useful animal model for a number of clinical and basic research applications.
Animals↗
Sources and fate of polychlorinated dibenzodioxins, dibenzofurans and related compounds in human environments.
Several of the major incidents resulting in potential human exposures to polychlorinated dibenzodioxins (PCDDs) and/or polychlorinated dibenzofurans (PCDFs), polychlorinated biphenyls (PCBs) and related compounds which have occurred in the U.S. in recent periods have resulted from improper disposal of hazardous chemical wastes. Prominent examples of such environmental contamination episodes are the Love Canal, into which ton quantities of chlorinated organic compounds containing substantial concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were deposited; numerous sites in the State of Missouri which were contaminated by the dumping of chlorinated organic wastes containing various PCDDs and possibly PCDFs, and PCBs; and the environs of a 2,4-D/2,4,5-T manufacturing plant site in Arkansas, which were contaminated with PCDDs. Environmental assessments of such sites have revealed extensive contamination of soils, waterways, fish and other biological species with these toxic compounds, which in turn could lead to human exposures. Other recently identified sources of PCDDs, PCDFs and related compounds in human environments include stack effluents from municipal refuse incineration, and fires and explosions involving electrical devices containing PCBs and polychlorinated benzenes. Data obtained in assessments of such incidents are presented, and the implications of these findings with respect to the distribution and persistence of PCDDs, PCDFs and related chemicals in the environment and possible effects on humans are discussed.
Accidents↗
Patient fat biopsies for chemical analysis and liver biopsies for ultrastructural characterization after exposure to polychlorinated dioxins, furans and PCBs.
A subset of workers was followed after exposure to polychlorinated biphenyls (PCBs), dioxins, and furans in an occupational medicine clinic setting. Patterns of PCBs found in adipose tissue resembled the pattern seen when soot from the incident or Aroclor 1254 was examined by GC-MS. Adipose tissue also revealed levels of hepta- and octachlorinated furans and dioxins as high as 8400 ppt in one repeatedly exposed worker. Control fat from patients with no known exposure to furans or dioxins was usually in the several hundred parts per trillion range for these isomers, but slightly over 2000 ppt in one sample. Electron microscopic analysis of liver biopsies from three patients who developed mild elevations of hepatic enzymes in their serum revealed morphologic alterations in some ways similar to those seen in animals after feeding experiments with PCBs, dioxins or the Binghamton State Office Building soot. These include pleomorphic mitochondria, giant mitochondria, prominent dense mitochondrial granules, cristae parallel to the long axis of the mitochondria and crystalline structure within same mitochondria as well as lipid droplets in liver cells and slightly dilated smooth endoplasmic reticulum.
Adipose Tissue↗
Occupational exposure to polychlorinated dioxins, polychlorinated furans, polychlorinated biphenyls, and biphenylenes after an electrical panel and transformer accident in an office building in Binghamton, NY.
A polychlorinated biphenyl (PCB) and tri- and tetrachlorinated benzene-containing electrical transformer was involved in an explosion and fire in a modern office building in Binghamton, New York, on February 5, 1981. Because of an unusual system of air shafts the entire building and adjacent garage became contaminated with toxic chemicals. Polychlorinated dioxins, furans, and biphenylenes were formed as pyrolytic by-products. Before the extent of the chemical contamination was appreciated workers were exposed to these chemicals. Four years after the explosion and after the expenditure of over $22 million for cleaning and other expenses, the building remains closed.
Accidents, Occupational↗
Medical surveillance of exposed persons after exposure to PCBs, chlorinated dibenzodioxins and dibenzofurans after PCB transformer or capacitor incidents.
The panel discussion from the perspective of occupational medicine regarding appropriate medical surveillance after a PCB transformer or capacitor incident is reviewed. A thorough occupational medicine history and physical examination is stressed for any worker or other patient who may have been exposed. Appropriate laboratory tests, including complete blood count with differential, serum chemistries, serial blood PCB determinations, fat biopsy to estimate furan and dioxin levels, if indicated, pulmonary function tests, chest X-rays, urinalysis including porphyrin measurement, nerve conduction velocity testing and other tests are discussed. No consensus was reached on recommended length of medical followup. Because the field is rapidly changing, yearly updates of medical protocols are warranted. In addition, the need for surveillance to be conducted by specialists with training and experience in the fields of occupational medicine and nursing was emphasized. It was stressed that measuring the chemicals and their levels in soot and air and then comparing these with the patient's blood or fat levels, in the case of PCBs, furans and dioxins, is vital. It was noted that at present no modality of treatment is known to be clinically efficacious in removing PCBs, furans and dioxins from tissues or blood.
Accidents, Occupational↗
Light and ultrastructural characteristics of neuroblastoma glioma hybrid NG 108-15 cells.
"Undifferentiated" neuroblastoma glioma hybrid NG 108-15 cells have not previously been characterized at a light and ultrastructural level despite their use in opiate receptor studies and their possession of one or more opioids. Three cell types rather than one were found. Type A is the classic round hybridoma cell. Type B is a neuron like cell and Type C is a giant cell similar to Type A cells but larger and with dense cytoplasm. Dense core vesicles, 800-1200 Ao in diameter were found as were virus particles in most Type A cells. Multivesicular bodies with clear vesicles which are interpreted as glutaraldehyde artefacts were found but no clear neurosecretory vesicles were found in any A cells--Etorphine at 10(-6) M for 48 hours and naloxone 10(-4) M were employed to product dependence and precipitated abstinence but no clear cut morphologic differences were noted between control, opiate dependent and precipitated abstinent cells.
Animals↗
Prolonged survival in bronchogenic carcinoma complicated by superior vena cava obstruction.
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Carcinoma, Bronchogenic↗
Acute hydrogen selenide inhalation.
Acute exposure to selenium hydrochloride resulted in severe dyspnea and a pneumomediastinum in a young healthy man. Pulmonary function tests revealed restrictive and obstructive airways disease. Although the patient's pulmonary function slowly improved, subsequent studies revealed persistent impairment. Therefore, exposure to selenium gas may result acutely in severe coughing and wheezing and may lead to irreversible obstructive lung disease.
Adult↗