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Halogenated Aromatic Poisoning: Introduction
(PCB, PBB, Dioxins, and others)
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Common persistent halogenated aromatics (PHA) include polychlorinated and polybrominated biphenyls (PCB, PBB), naphthalenes, benzenes, and diphenyl ethers (PCDE, PBDE), as well as a number of pesticides such as DDT ( Chlorinated Hydrocarbon Compounds). Unwanted byproducts formed during manufacture and heating or burning of chlorophenoxy herbicides ( Herbicide Poisoning: Introduction), chlorophenols ( Pentachlorophenol Poisoning: Introduction), or PCB include polychlorinated dibenzofurans (PCDF) and dibenzo-p -dioxins (PCDD). Triclosan is a hydroxylated PCDE commonly used in household products as a bacteriostat. PBDE are increasingly common in the environment due to their wide use as flame retardants in plastics and electronic components. PCB, marketed in the USA as Aroclors, are the most environmentally abundant of the halogenated aromatics and are still found in products from North America, Western Europe, or Japan produced before 1979. PCB manufacture and use continued in other areas up to the 1990s. The most common PCB-containing products still in use include electrical transformers and capacitors and fluorescent light ballasts. These should be considered to contain PCB if manufactured before 1980 unless they are labeled to the contrary. Other uses resulting in persistent contamination around farms and small animal facilities include hydraulic and heat transfer fluids, epoxy paints, and construction adhesives.
Polyhalogenated aromatics are chemically stable, lipid soluble, and bioaccumulative. They are rapidly absorbed by all routes of exposure and accumulate in adipose tissue, from where they are gradually eliminated during fat mobilization. Persistence, bioaccumulation, types of toxic effects, and potencies vary considerably among the many different compounds. PCB, PCDF, PCDD, and naphthalenes are always present as mixtures. Typically, representatives from all 4 classes as well as halogenated aromatic pesticides are present.
Livestock feed and pet food contamination as well as fish and fish meal were previously considered the major sources of exposure. It is now known that airborne (vapor phase) and forage exposures are nearly universal, although at considerably lower levels.
Most toxic effects of halogenated aromatics are subtle and delayed, but may be additive. Effects may include: 1) wasting (weight loss not necessarily accompanied by decreased food consumption; however, complex environmental mixtures with net antiestrogenic activity may increase food consumption, body weight and body fat), 2) skin disorders (chloracne, edema, alopecia, hyperkeratosis), 3) immune suppression, 4) enlarged liver with fatty change and enzyme induction, 5) endocrine disruption (antiestrogenicity; hypothyroxinemia, often without an increase in TSH), 6) reproductive disorders (abnormal cycling, reduced conception, fetotoxicity and fetal resorption, teratogenesis), and 7) carcinogenesis. Birds and guinea pigs are particularly susceptible to effects mediated by the Aryl hydrocarbon receptor (AhR), while hamsters and voles are more resistant. The most prevalent halogenated aromatics are noncoplanar, have little affinity for the AhR, and cause health effects by multiple mechanisms. They induce a different profile of xenobiotic metabolizing enzymes than do AhR agonists and tend to be weakly estrogenic rather than antiestrogenic. Noncoplanar PCB also inhibit gonadal and (probably) adrenal gland steroidogenesis. Fertility can be decreased by both coplanar and noncoplanar compounds. The less chlorinated and ortho-rich PCB stimulate ryanodine-sensitive intracellular calcium channels (see also malignant hyperthermia, Malignant Hyperthermia : Introduction) and have a number of subtle effects on learning, memory, and behavior. These PCB are at higher proportions in the vapor phase, forages, and in many fish.
A unique hyperplastic gastritis has been observed in monkeys, swine, and rats exposed to PCB. Erosions in the mucosa are accompanied by autophagous parietal cells with mucus-secreting cells becoming dominant. These changes appear to be of systemic origin rather than from direct gastric irritation. Cattle with a high PCB burden (PCB-containing oil in back rubbers) became ill and suffered mortality when shipped; there were severe intestinal hemorrhages which may be a later stage of the stomach inflammation in monogastric species. Although weight gain may appear normal, decrements in feed efficiency have been demonstrated in swine.
Many effects are subtle and may not become apparent until the animal is stressed or, in the case of prepubertal exposure, reaches adulthood. There are no diagnostic signs specific to these broad-acting and subtle poisons; diagnostic confirmation relies on chemical analysis suggested by the clinical history. Initial diagnosis is based on a complete history, visual inspection of the premises for potential exposures, and elimination of more common etiologies. These compounds are readily detected in serum or whole blood as well as body fat, milk fat, liver, feed, and other suspected sources. Fluid samples for residue analysis should be collected in clean, acetone-rinsed glass or stainless steel containers with caps lined with acetone-rinsed teflon or aluminum foil. Solid samples may be wrapped in aluminum foil and frozen. The dull side of the foil should be in contact with the sample; the shiny side is coated with waxes that interfere with the analysis. Plastics should be avoided.
Treatment is most likely to be beneficial when instituted as soon as possible following acute exposure. It is based on discovering and eliminating the source of exposure, bathing animals with detergent and cool water after dermal exposure (do not scrub vigorously). Repeated large oral doses of activated charcoal (1-4 g/kg small animals; 1-2 g/kg large animals) or gastric lavage may be of benefit after oral exposure. The charcoal will trap some PHA in the intestine preventing absorption into the body and reducing fatty tissue concentrations. Also, oral activated charcoal can trap some PHA mobilized from the fat and excreted in bile into the intestines, thus preventing re-uptake and reducing the body burden. It is important to minimize stress and optimize environmental conditions following severe exposures. Residue levels above the MRL make these livestock unsaleable. For breeding stock and pets, elimination is hastened by weight loss, parturition, or lactation. Offspring, which are usually exposed in utero if the mother encounters PHA while pregnant, should not be suckled from contaminated mothers. Studies in humans suggest physical, reproductive, cognitive, concentration, and social deficits in offspring of mothers, long after exposure. This suggests that animals may be of doubtful value as breeding stock. Males, if suitably fertile, should remain useful.

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