Phosgene (CG) is a highly irritant gas widely used industrially as a chemical intermediate for the production of dyes, pesticides, and plastics, and can cause life-threatening pulmonar y edema within 24 hours of exposure. This study was designed to investigate acute changes in lung tissue histopathology and selected bronchoalveola r lavage uid (BALF) factors over time to determine early diagnostic indicators of exposure. Three groups of 40 male mice each were exposed to 32 mg/m 3 (8 ppm) CG for 20 minutes, and 3 groups of 40 control male mice were exposed to ltered room air for 20 minutes, both exposures were followed by room air washout for 5 minutes. At 1,4,8,12,24, 48, and 72 hours after exposure each group of mice was euthanized and processed for histopatholog y, bronchoalveola r lavage or gravimetric measurements , respectively. Over time, the histopathologica l lesions were characterized by acute changes consisting of alveolar and interstitial edema, brin and hemorrhage , followed by signi cant alveolar and interstitial ooding with in ammatory cell in ltrates and scattered bronchiolar and terminal airway epithelial degeneratio n and necrosis. From 48 to 72 hours, there was partial resolution of the edema and degenerative changes, followed by epithelial and broblastic regeneration centered on the terminal bronchiolar areas. Bronchoalveola r lavage was processed for cell differential counts, LDH, and protein determination. Comparative analysis revealed signi cant increases in both postexposur e lung wet/dry weight ratios, and early elevations of BALF LDH and protein, and later elevations in leukocytes. This article describes the use of histopathology to chronicle the temporal pulmonary changes subsequent to whole body exposure to phosgene , and correlate these changes with BALF ingredients and postexposur e lung wet weights in an effort to characterize toxic gas-induced acute lung injury and identify early markers of phosgene exposure.

The quality control of wastewater treatments was monitored using selected novel and classical physicochemical and microbiological indicators, and the associations of the treatments with the effluents was analyzed. The microbiological indicators monitored were heterotrophic plate count (HPC), total coliforms (TC), fecal coliforms (FC), fecal streptococci (FS), sulfite-reducing clostridia (SRC), Pseudomonas aeruginosa, and Salmonella spp. The stages of wastewater treatment also were evaluated through determination of ammonia; biological oxygen demand (BOD(5)); chemical oxygen demand (COD); chloride; conductivity; suspended dissolved and total solids; fats; nitrate, nitrite, and total nitrogen; pH; phosphate and total phosphorus. Additional indicators included the Escherichia coli growth inhibition (IGEC) bioassay for assessing whole effluent toxicity, spectral determinations between wavelengths (lambda) 190-650 nm, and total (TP) and soluble (SP) protein contents. Of the more common physicochemical parameters, only BOD(5), COD, suspended and total solids, and fats showed a statistically significant reduction between raw water and effluent; for the microbiological indicators, significant reduction was seen only for HPC, FC, and Ps. aeruginosa. We suggest that determinations of Ps. aeruginosa be commonly used as an indicator of wastewater quality. Spectral analysis--most notably the values of absorbance at 225, 255, and 295 nm-revealed a statistically significant correlation with several physicochemical parameters. Statistical analysis of SP and TP values showed them to be good indicators of contamination. The quantitative study of Salmonella spp. and the results of the IGEC bioassay show the need for close control of infectious and toxic risks in wastewater and effluents.

Background/aims: The euthymic hairless guinea pig was the animal model of choice at this laboratory for vesicant injury research. The supply of these animals, however, was interrupted in 1993 by an outbreak of Lisferia monocyfogenes at the commercial supplier's breeding facility, thereby forcing a search for alternative animal models. This report describes the development of a weanling pig model for use in evaluating the severity of skin lesions induced by sulfur mustard [bis(2‐chloroethyl)sulfide; SM] using a variety of bioengineering techniques. These methods include reflectance colorimetry (erythema response), high frequency ultrasound imaging (edema response) and a modified dermal torque meter procedure to test for Nikolsky's sign (damage at the dermal‐epidermal junction). The time course and exposure time‐dependence of SM‐induced lesions for these parameters were characterized in this model and compared with previous results in the haired and hairless guinea pig. Methods: Six male Yorkshire Cross pigs (7–10 kg) were used in this study. The hair on the dorsal surface of each animal was shaved the afternoon prior to SM exposure. Twenty‐four dorsal skin sites on each pig were exposed to saturated SM vapor (1.4 mg/l) using 14‐mm diameter vapor cups for 0 (control), 5, 10, 15, 20, or 25 min, with four sites per exposure level. Control and exposure sites were rotated to prevent site‐specific biases. Lesions were evaluated for erythema (reflectance colorimeter) at 4, 6, 12, 24 and 48 h post‐exposure, and for edema (high frequency ultrasound) at 6, 12, 24, and 48 h post‐exposure. Evaluations for Nikolsky's sign and histopathology were conducted at 48 h post‐exposure. Results: Maximum erythema responses occurred at 24 h postexposure for all SM exposure times (5, 10, 15, 20 and 25 min). The overall maximum response occurred with a 15‐min SM vapor exposure at 24 h post‐exposure. Exposures longer than 15 min did not induce significantly greater erythema at any of the time points examined. The earliest time point at which significant edema was noted was at 12 h for the 15‐ and 25‐min SM vapor groups. Maximum edema occurred at 48 h following a 15‐min exposure. No significant increase in edema was noted at any observation time point with exposures longer than 15 min. All sites showed a weakening of the dermal‐epidermal junction (positive Nikolsky's sign) 48 h after a 15‐min or longer SM vapor challenge. The histologic severity of the lesions did not significantly worsen as the vapor exposure was increased beyond 15 min. (Following a 15‐min SM exposure, incidences of epidermal necrosis, pustular epidermitis, microblisters and vascular damage had reached 100%, with maximum mean severity scores.) The weanling pig is more resistant to the effects of SM vapor than either the haired or hairless guinea pig, showing a delayed response and requiring a longer exposure time to generate the same (quantitative and qualitative) response in erythema, Nikolsky's sign and microblister formation. SM vapor‐induced edema formation in the wean...

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