Asbestos content of lung tissue in patients with malignant peritoneal mesothelioma: A study of 42 cases.

Lung tissue from 42 peritoneal mesothelioma cases was analyzed by light microscopy and scanning electron microscopy/energy dispersive spectrometry. There were 34 men and 8 women with a mean age of 61 ± 10 years. Also, 17% of cases had histologically confirmed asbestosis, and 26% had only parietal pleural plaques. The asbestos body count exceeded our normal range in 22 of 42 cases (52%). Cases with asbestos-related pulmonary disease had higher fiber burdens than those without. The vast majority of fibers were commercial amphiboles (amosite with lesser amounts of crocidolite). These findings concur with previously published epidemiological observations.

Malignant mesothelioma not related to asbestos exposure: Analytical scanning electron microscopic analysis of 83 cases and comparison with 442 asbestos-related cases.

Epidemiological studies indicate that 80-90% of mesotheliomas are asbestos related. This suggests that 10-20% are not. Lung fiber burden analysis provides objective information about past exposures to asbestos. We have performed lung fiber burden analysis on a large cohort of mesothelioma cases and compared the findings with a reference population. Herein we report our findings along with demographic and exposure data.

Immunostaining in lung cancer for the clinician. Commonly used markers for differentiating primary and metastatic pulmonary tumors.

Immunohistochemical stains have become invaluable for the diagnosis of pulmonary malignancies (both primary and metastatic), particularly given the small size of transbronchial and endobronchial biopsies and the increasing need to conserve tissue for molecular studies. There are many panels of immunostains currently available to help differentiate between common types of pulmonary malignancies. It is the purpose of this review to summarize some of the most commonly used immunostains for the distinction of primary pulmonary malignancies from one another in areas with histological overlap and for distinguishing primary pulmonary malignancies from other cancers with which they may be confused. These include differentiating between poorly differentiated adenocarcinoma and poorly differentiated squamous cell carcinoma, small cell/large cell neuroendocrine carcinoma and basaloid carcinoma, and primary and metastatic adenocarcinoma involving the lung. In addition, we address the distinction between mesothelioma and pulmonary adenocarcinoma. Pitfalls in the use of these markers are also addressed. Although not aiming to be comprehensive, this review aims to guide and influence common practice by furthering the clinician's knowledge on using immunohistochemical stains for characterization of pulmonary neoplasms. This summary of frequently used immunohistochemical stains can provide usefulness by allowing accurate characterization of pulmonary tumors, thereby allowing for conservation of tissue for additional molecular testing.

In vitro nephrotoxicity induced by propanil.

Propanil is a postemergence herbicide used primarily in rice and wheat production in the United States. The reported toxicities for propanil exposure include methemoglobinemia, immunotoxicity, and nephrotoxicity. A major metabolite of propanil, 3,4-dichloroaniline (3,4-DCA), has been shown to be a nephrotoxicant in vivo and in vitro, but the nephrotoxic potential of propanil has not been examined in detail. The purpose of this study was to determine the nephrotoxic potential of propanil using an in vitro kidney model, determine whether in vitro propanil nephrotoxicity is due to metabolites arising from propanil hydrolysis, and examine mechanistic aspects of propanil nephrotoxicity in vitro. Propanil, 3,4-DCA, propionic acid (0.1-5.0 mM), or vehicle was incubated for 15-120 min with isolated renal cortical cells (IRCC; approximately 4 million cells/mL) obtained from untreated male Fischer 344 rats. Cytotoxicity was determined by measuring lactate dehydrogenase release from IRCC. In 120-min incubations, propanil induced cytotoxicity at concentrations >0.5 mM. At 1.0 mM, propanil induced cytotoxicity following 60- or 120-min exposure. Cytotoxicity was observed with 3,4-DCA (2.0 mM) at 60 and 120 min, while propionic acid (5.0 mM) induced cytotoxicity at 60 min. In IRCC pretreated with an antioxidant, cytochrome P450(CYP) inhibitor, flavin adenine dinucleotide monooxygenase activity modulator, or cyclooxygenase inhibitor before propanil exposure (1.0 mM; 120 min), only piperonyl butoxide (0.1 mM), a CYP inhibitor, pretreatment decreased propanil cytotoxicity. These results demonstrate that propanil is an in vitro nephrotoxicant in IRCC. Propanil nephrotoxicity is not primarily due to metabolites resulting from hydrolysis of propanil, but a metabolite resulting from propanil oxidation may contribute to propanil cytotoxicity.