Subcutaneous Edema

A significant increase in the incidence of fetal soft-tissue and skeletal anomalies was seen following treatment of pregnant rats with HCDD at the 100 jug/kg/day dose level. The incidence of cleft palate, subcutaneous edema, vertebrae with split or unfused centra, and split sternebrae was significantly greater than among control litters or the control fetal popu-... 

OCDD. Signs of maternal toxicity were not observed in rats given 100 or 500 mg/kg/day OCDD. Examination of the fetuses did not reveal changes in fetal body measurements, incidence of fetal resorptions, or incidence of any fetal anomaly among litters or the fetal population. At 500 mg/kg/day, the incidence of subcutaneous edema was significantly increased among the fetal population (23/100 compared with 8/156 in controls) but not among litters (9/18 compared with 6/28 in controls). 

Severe dyspnea, subcutaneous edema, and distended abdomens were observed in some birds receiving 1 or 10 fig 2,3,7,8-TCDD/kg/day. Dyspnea and mucus accumulation in the mouth prior to death were observed in birds receiving 100 fig 2,3,7,8-TCDD/kg/day. No overt clinical signs were observed in birds receiving OCDD. 

Signs and Symptoms Causes fever, labored breathing with increased respiratory rate, and depression. There may be paroxysmal coughing. May cause conjunctivitis, subcutaneous edema of the head, neck, brisket, thorax, and ventral abdomen. There may be edema in the supraorbital fossa above the eye. 

Postmortem findings include edema in the periorbital tissue, neck muscles, ligamentum nuchae, intermuscular and lungs hemorrhage of the tongue, intestinal serosa, kidneys, and pericardium and general subcutaneous edema and hemorrhage. 

The approximate lethal dose for skin absorption in pregnant rats and rabbits was 7.5 and 5.0g/kg, respectively Cutaneous application of DAIAC resulted in a marked incidence of embryo mortality at doses that did not affect maternal body weight or produce any signs of maternal toxicity. Teratogenic effects (three fetuses from one dam with encephalocele one of eight with diffuse subcutaneous edema) were found in rats only when DMAC was applied on gestation days 10 and 11 at a total dose of 2400 mg/kg. In another study, DMAC administered... 

Given orally to pregnant rats at doses ranging from 5 to 50mg/kg body weight/day, purified pentachlorophenol produced dose-related signs of fetotoxicity, including resorptions, subcutaneous edema, dilated ureters, and anomalies of the skull, ribs, and vertebrae. "... 

Developmental Effects. Oral developmental toxicity studies of deca-, octa-, and pentaBDE have shown no evidence of teratogenicity in animals. Gestational exposure to a high (1,000 mg/kg/day) but maternally nontoxic dose of decaBDE was fetotoxic in rats as shown by subcutaneous edema and delayed skull bone ossification. Commercial mixtures of octaBDE caused skeletal ossification variations in rats and rabbits at maternally toxic levels and other indications of fetotoxicity at lower doses. Effects of gestational exposure to octaBDE included minimally increased postimplantation loss in rats at >10 mg/kg/day, increased resorptions in rats at 25 mg/kg/day, and increased skeletal variations in rabbits at 15 mg/kg/day and rats at 50 mg/kg/day. No evidence of fetotoxicity was found in the only available study of pentaBDE in rats at maternally toxic doses < 200 mg/kg/day. No studies are available on developmental effects of PBDEs in humans. Based on the evidence in animals, PBDEs are unlikely to cause developmental toxicity at expected levels of exposure. 

Chick edema disease became a serious economic problem by the mid-1950s, by which time millions of broilers had succumbed to it in the U.S. The problem was traced to toxic components in the unsaponifiable fraction of certain low cost feed fats Introduced into the chick diet to increase the caloric intake (ref. 121c). Symptoms included fluid in the heart sack and abdominal cavity, subcutaneous edema and liver necrosis. Injection of purified chick edema factor into fertile eggs resulted in lower hatch yield, embryonic deformities and edema. Unhatched embryos exhibited a variety of defects (malformed beaks, leg deformities, no development of the right mesencephalon, and eye defects). Hatched embryos were growth-retarded, with sparse and defective feathers. The isolated toxin was ultimately identified as 1.2,3,7.8,9-... 

Hepatonephritis and pulmonary edema were reported as causes of fetal death. The presence of PCE in breast milk was the cited reason for obstructive jaundice in a 6-week old infant (ref. 35. P 303). A study by Schwetz et al. (ref. 68) indicates that PCE may be teratogenic. Delayed skull-bone ossification and split stembrae were observed in mice, as well as increased fetal resorption, decreased fetal body weight and fetal subcutaneous edema. 

F (periorbital edema, facial alopecia, squamous metaplasia, hyperkeratoses subcutaneous edema)... 

Rat (Sprague-Dawley) 10 d Gd 6-15 1 x/d (GO) 0.1 1 (subcutaneous edema) 10 (growth retardation, dilated renal pelvis, delayed ossification) Schwetz et al. 1973 HCDD5... 

Some common developmental effects attributed to 2,3,7,8-TCDD exposure in most laboratory mammals are thymic hypoplasia, subcutaneous edema, decreased prenatal growth, and prenatal mortality (Couture et al. 1990). In addition, there are other species-specific effects, such as cleft palate in mice. Any of... 

Developmental toxicity has also been observed in animals exposed to other CDDs. These effects include heart defects in rats exposed to 2,7-DCDD (Schwetz et al. 1973) decreased thymic weight in rats exposed to 1,2,3,7,8-PCDD (Madsen and Larsen 1989) subcutaneous edema, decreased fetal growth, delayed ossification, dilated renal pelvis, and cleft palate in rats exposed to HxCDD (Schwetz et al. 

Subcutaneous edema Papulovesicular rash Vesication (bullae) Inflammatory hyperpigmentation... 

Drucker Y, Prayson RA, Bagg A, Calabrese LH. Lymphocytic vasculitis presenting as diffuse subcutaneous edema after hepatitis B virus vaccine. J Clin Rheumatol 1997 3 158-61. 

Complement deficiencies are associated with several diseases. Alternative pathway deficiencies are rare, but when they exist more than one-half of factor D or properdin-deficient individuals suffer from Neisseria infections of which 75% are fatal. Individuals with deficiencies in the MAC components, e.g., C5, C6, Cl, and C8, are also susceptible to infection with Neisseria. Deficiencies in C1, C4, and C2 are associated with systemic lupus erythematosus and glomerulonephritis. Hereditary angioedema, a disease characterized by recurrent submucosal and subcutaneous edema, is caused by a deficiency in Cl inhibitor. Complexes and interactions similar to those of the complement system are also characteristic of the clotting system (Chapter 36). 

In ruminants, typical clinical manifestations are loss of condition, diarrhea, subcutaneous edema, profound weakness and jaundice. Furthermore, pathological... 

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