Candace S. Wheeler

Increased 5-lipoxygenase metabolism in the lungs of human subjects exposed to ozone

The environmental pollutant ozone, at sufficiently high levels, is known to induce pulmonary inflammation with resultant airway obstruction in normal subjects. Eicosanoids comprise one group of mediators released from alveolar macrophages which are involved in the pathogenesis of inflammatory lung diseases. We compared the effects of 2-h exposures to 0.4 ppm ozone and filtered air on pulmonary function and eicosanoid levels in bronchoalveolar lavage fluid in 11 normal healthy volunteers. Subjects were exposed to a 6-fold increase in minute ventilation using an adjusted work load on a cycle ergometer. All subjects complained of cough and dyspnea, and demonstrated increased airway obstruction, and increased specific airway resistance following ozone exposure as compared to air exposure. Bronchoalveolar lavage cell count demonstrated a 9-fold increase in the number of neutrophils with a lesser reduction in the number of alveolar macrophages following ozone exposure. Notably, bronchoalveolar lavage fluid leukotriene (LT) C4 (8-fold) and to a lesser extent LTB4 (1.5-fold) levels were higher following ozone exposure compared to air control, with no change in prostaglandins. In a subset of four subjects, alveolar macrophage arachidonic acid metabolism was studied in vitro following separate in vivo exposures to both ozone and air. Alveolar macrophages obtained following ozone exposure released more 5-lipoxygenase (1.5-fold) metabolites, with no change in cyclooxygenase metabolites, than did cells obtained following air exposure. These observations document activation of the 5-lipoxygenase pathway in the lung following ozone exposure, and suggest that alveolar macrophages may participate in the generation of LT, whose actions promote airway inflammation and obstruction.

Cellular, biochemical and functional effects of ozone: new research and perspectives on ozone health effects.

Ozone, a toxic component of photochemical oxidant air pollution, has been the focus of considerable research efforts for several decades. In spite of this large body of work, questions remain as to the potential risks to human health represented by chronic low-level exposure to ozone. Newer studies in animals have provided fundamental information on the range of biochemical, functional and morphologic responses to ozone exposure. While the response to ozone exposure is extremely complex, some generalities have emerged which may aid attempts to apply the results of these studies to decisions regarding the protection of human health.

SCREENING STUDY TO EVALUATE SHREDDER RESIDUE MATERIALS

The Vehicle Recycling Partnership (VRP) initiated feasibility studies to evaluate the use of automated separation processes to recover plastics and polyurethane (PU) foams from shredder residue. One of the prevailing issues impeding the commercial success of these processes is contamination of the shredder materials. The contaminants include dirt, oils, glass, metal fines, polychlorinated biphenyls (PCBs) and heavy metals. The presence of PCBs and heavy metals was determined in a number of mixed plastics and PU foam samples separated using an automated separation process. An aqueous cleaning approach was investigated using various commercial surfactants to determine their effectiveness for removing oils, PCBs, and heavy metals. Mass balances of processed and cleaned materials were calculated to determine the cleaning efficiencies of the various surfactants.

The Effect of Aramid and Metaphosphate Fibers on Macrophage Viability and Function

This study was designed to evaluate the cytotoxicity of a number of asbestos substitute fibers on primary rat alveolar macrophages (AMs) and a mouse macrophage-Iike cell line (J774A.1) in vitro. Following 24- and 48-hour incubations, the cells were observed under phase contrast microscopy for changes in cell morphology and cell viability was assessed using trypan blue exclusion. A viability index (VI) was calculated to reflect changes in both cell number and cell viability. All of the materials studied produced a concentration-dependent reduction in VI. In addition, both Kevlar and calcium sodium metaphosphate (CSMP) fibers produced a concentration- dependent release of lactate dehydrogenase (LDH) from primary AMs. Finally, no chemotaxis was observed in response to either Kevlar or CSMP fiber alone, but both fibers stimulated measurable concentration-dependent chemotaxis when incubated with AMs. These results suggest that all of the materials were cytotoxic to AMs in vitro in the form and at the concentrations (25, 250 µg/mL) used in this study and can affect AM function. What effect these materials have on the human health remains to be determined.