Nitrogen dioxide (NO2) is a product of combustion that has become recognized as a significant component of indoor air in some homes. Despite extensive study, it remains unresolved whether exposures to low levels of NO2 affect airway function or reactivity. These studies were designed to assess effects of various levels and patterns of NO2 exposure on pulmonary function and airway reactivity in normal humans. Normal volunteers screened for the absence of airway hyperreactivity were exposed for 3 h in an environmental chamber to purified air or NO2, separated by at least 2 wk, according to three protocols: (1) continuous 0.60 ppm NO2, (2) baseline 0.05 ppm NO2 with intermittent peaks of 2.0 ppm, and (3) continuous 1.5 ppm NO2. Subjects exercised for 10 min of each 30 min at a level sufficient to result in a minute ventilation near 40 L/min. Pulmonary function was measured before, during, and after exposure. Airway reactivity to increasing doses of carbachol was assessed 30 min after exposure. NO2 did not directly alter pulmonary function in any of the exposure protocols. In addition, airway reactivity was not altered by continuous exposure to 0.60 ppm or intermittent peaks of 2.0 ppm NO2. In contrast, continuous exposure to 1.5 ppm NO2 resulted in a greater fall in FVC and FEV1 in response to carbachol than after exposure to air (percent decrease in FVC: 1.5% after air, 3.9% after NO2, p less than 0.01). We conclude that for subjects without airway hyperreactivity, exposure to 1.5 ppm NO2 for 3 h increases airway reactivity, whereas repeated 15-min exposures to 2.0 ppm NO2 do not alter airway reactivity.

Studies were performed with an interest in determining a pressure threshold for extracorporeal shock wave induced renal damage. Histological evidence of intraparenchymal hemorrhage was used as an indicator of tissue trauma. Depilated C3H mice were anesthetized and placed on a special frame to enhance visualization and treatment of the kidneys in situ. A Wolf electrohydraulic generator and 9 French probe designed for endoscopic use were utilized to expose the kidneys to 10 double spherically divergent shock waves. Measurements of the shock waves revealed two positive pressure peaks of similar magnitude for each spark discharge. The kidneys were exposed to different peak pressures by choice of distance from the spark source and were removed immediately after treatment for histologic processing. A dose response was noted with severe corticomedullary damage apparent following 15 to 20 MPa shocks. Hemorrhage was more apparent in the medulla where evidence of damage could be seen following pressures as low as three to five MPa. When a latex membrane was interposed to prevent possible collapse of the initial bubble from the spark source against the skin surface, histological evaluation revealed substantial reduction of severe tissue damage associated with the highest pressures tested, 20 MPa. However, the threshold level for evidence of hemorrhage remained about three to five MPa. Hydrophonic measurements indicated that the membrane allowed transmission of the acoustic shock waves and suggested that collapse of the bubble generated by electrohydraulic probes may have local effects due to a cavitation-like mechanism.

Plasma plant sterol concentrations (an index of cholesterol absorption efficiency) and plasma lathosterol concentration (an index of cholesterol synthesis rate) were measured in 52 patients with non-insulin dependent diabetes mellitus (NIDDM) and 36 non-diabetic controls. Plasma plant sterol concentrations were significantly (P less than 0.01) lower in diabetic patients (campesterol: men -36%, women -48%; betasitosterol: men -35%, women -42%). Fasting serum insulin levels were inversely correlated with plasma plant sterol concentrations in diabetic patients (campesterol: r = -0.347, P = 0.012; betasitosterol: r = -0.345, P = 0.012) and in non-diabetic men (campesterol: r = -0.578, P = 0.039; betasitosterol: r = -0.702, P = 0.008). Serum insulin levels were also correlated significantly with plasma lathosterol concentration in diabetic patients (r = 0.295, P = 0.034). The results of this study suggest that absorption of plant sterols and possibly cholesterol from the diet may be reduced in hyperinsulinemic diabetics.

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et al., 1985; NTP, 1993; Nikula et al., 1995;Heinrich et al., Inhaled CdCl 2 is a pulmonary carcinogen in rats but not in mice. 1995). Different strains of rats and mice have been used We hypothesized that pulmonary metallothionein (MT) induction in the different studies with cadmium and solid particles, may be different in both species and thereby may lead to different including the standard strains for chronic NTP bioassays, levels of protection from Cd-induced lung injury. Fisher-344 rats and i.e., Fischer-344 rats and B6C3F 1 mice. The species-specific B6C3F 1 mice were exposed for 4 weeks to CdCl 2 aerosols of 0, 30, lung tumor response was found in all of them and we de- cided, therefore, to use those standard strains in our subseAnimals from each exposure group were terminated at 1, 30, and quent studies. With respect to particle-induced lung tumors 133 days after the end of exposure. The lungs were lavaged for cell in rats, a condition of lung particle overload is thought to and biochemical analyses. Cadmium and MT in lavagate and lung tissue were measured. The retention half-time of pulmonary Cd was be the basis (Oberdörster, 1995), yet this condition does not greater in mice (290 vs 90 days, p õ 0.05). Cd exposure provoked occur after low-level Cd exposure. Thus, the reasons for an inflammatory response which was dose-dependent in both species, these species differences in tumorigenic response to inhaled and while it was only short-lived in rats, it persisted throughout the Cd are not known yet and studying them provides a unique observation period in mice at the high exposure concentrations. Mice opportunity to gain a better understanding of the mechanisms were found to have a greater baseline level of MT (18.04 { 6.96 vs important for Cd carcinogenesis, which may include species 11.7 { 1.98 mg MT/g control lung, p õ 0.05). Mice showed greater differences in metallothionein (MT) induction and turnover. inducibility of MT for a given CdCl 2 exposure concentration; how-MT is a low-molecular-weight protein which is highly ever, both species had a similar relationship between retained pulmoconserved throughout the animal kingdom. The major role nary Cd and MT induction though mice maintained increased MT levels for a longer period of time. The greater pulmonary baseline of MT appears to be its involvement with essential metal MT together with the longer presence of Cd-induced pulmonary MT homeostasis, specifically its physiologic association with may result in greater protection from Cd carcinogenicity in spite of zinc and copper metabolism. It has also been suggested that the greater pulmonary Cd-induced inflammation in mice. ᭧ 1996 MT plays a role in protecting cells from heavy metal toxicity Society of Toxicology(e.g., Cd, Hg) and oxidant stresses and, moreover, that MT may protect cells from the carcinogenic effect of Cd by sequestering Cd. The reader is referred to several reviews Inhaled cadmium (Cd) has been linked with lung cancer in for further details of the role of MT with respect to heavy human...

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