White phosphorus lesion

Fig. 4.64 White phosphorus lesion (Brulure Chimique, Centre de Traitement des Brules, HIA Percy. Qamart,...

In rats exposed for an intermediate duration to an unknown concentration of airborne white phosphorus from the furnace room of a phosphorus factory, an increase in permeability of capillary walls, lesions in the walls of blood vessels, and evidence of impaired microcirculation were observed in the mouth (Ruzuddinov and Rys-Uly 1986). Severe damage to the oral mucosa was also observed in these animals. No information regarding effects on the heart was located in the animal studies. 

No effects on pregnancy rate or number of pups born alive were observed following the mating of male rats exposed to 1,742 mg orthophosphoric acid equivalents/m3 of white phosphorus smoke 15 minutes/day, 5 days/week for 10 weeks with female rats exposed for 3 weeks (similar exposure protocol) (Brown et al. 1981 Starke et al. 1982) or the mating of male rats exposed to 1,742 mg orthophosphoric acid equivalents/m3 15 minutes/day, 5 days/week, for 13 weeks to unexposed female rats (Brown et al. 1981 Starke et al. 1982). No exposure-related lesions were seen in the testis, epididymis, ovary, and uterus of rats exposed to 1,742 mg orthophosphoric acid equivalents/m315 minutes/day, 5 days/week, for 13 weeks (Brown et al. 1981). 

In the only chronic duration oral study in animals, no treatment-related histopathological lesions were observed in the lungs or other organs (not otherwise specified) in rats given <1.6 mg/kg/day white phosphorus in the diet for up to 479 days (Fleming et al. 1942). Only six rats per dose group were used. 

White Phosphorus Smoke. There is limited information on the neurotoxicity of white phosphorus smoke. No human exposure studies were located. No lesions were observed in the brains of rats exposed to 1,742 mg orthophosphoric acid equivalents/m3 of white phosphorus smoke 15 minutes/day, 5 days/week for 13 weeks (Brown et al. 1981). No other studies examining neurological end points were observed. 

Qualitative in-life biomarkers that are characteristic of chronic exposure to white phosphorus include progressive destruction of the jaw bones (phossy jaw), brittleness of long bones, and poor healing of oral cavity lesions including tooth sockets after tooth extraction (see Section 2.2 for details). In-life biomarkers that are probably shared with other toxic compounds include increased permeability of capillary walls and impaired microcirculation. Postmortem qualitative biomarkers include hyperkeratosis of the epithelium of the oral mucosa and lesions of the capillary walls (see Section 2.2 for details). Hyperkeratosis is a microscopic morphological finding that can be seen in biopsy material from a living patient or from an autopsy and is seen in association with phosphorus intoxication. 

White Phosphorus Smoke. No reproductive performance effects or histological lesions on reproductive tissues were observed in male and female rats exposed to white phosphorus smoke for intermediate durations (Brown et al. 1981). A limitation of this study is that the rats were exposed for a very short daily duration (15 minutes/day). Studies that involved longer daily inhalation exposures or dermal exposures would be useful to determine the potential for reproductive toxicity in humans exposed to white phosphorus smoke. 

White Phosphorus Smoke. Information on the neurotoxicity of white phosphorus smoke is limited to an intermediate-duration study that examined the brain for histological lesions (Brown et al. 1981). Inhalation and dermal exposure studies examining a battery of neurological end points (including neurobehavioral effects) would be useful in assessing the neurotoxic potential of white phosphorus smoke. 

The principal form of toxicity of absorbed elemental phosphorus, a destructive jaw process (phossy jaw), has been virtually eliminated by using (a) less white phosphorus in all industrial settings other than the military and (b) efficient adjunctive dental screening of exposed individuals for periods of up to 2 years postexposure. Careful dental screening consists of regular radiological assessment of the mandible for characteristic lesions, early and aggressive treatment of those lesions, and absolute prohibition of further phosphorus exposure.33... 

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