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The highest monoterpene concentration (GM), in the breathing zone, measured during processing of pine, was less than one-fourth of the Finnish occupational exposure limit (OEL, 570 mg/m(3)). Verbenol concentrations in postshift urine samples reflected accurately the exposure to monoterpenes. The concentrations of inhalable dust (GM) were less than one-half the Finnish OEL (5 mg/m(3)). No significant differences in dust exposure were observed among tree species processed. Work-related symptoms appeared to correlate with monoterpene exposure during processing of pine and with wood dust exposure during processing of spruce.

Repeated airway exposure to wood dust has long been known to cause adverse respiratory effects such as asthma and chronic bronchitis and impairment of lung function. However, the mechanisms underlying the inflammatory responses of the airways after wood dust exposure are poorly known. We used a mouse model to elucidate the mechanisms of particle-induced inflammatory responses to fine wood dust particles. BALB/c mice were exposed to intranasally administered fine (more than 99% of the particles had a particle size of < or = 5 microm, with virtually identical size distribution) birch or oak dusts twice a week for 3 weeks. PBS, LPS, and titanium dioxide were used as controls. Intranasal instillation of birch or oak dusts elicited influx of inflammatory cells to the lungs in mice. Enhancement of lymphocytes and neutrophils was seen after oak dust exposure, whereas eosinophil infiltration was higher after birch dust exposure. Infiltration of inflammatory cells was associated with an increase in the mRNA levels of several cytokines, chemokines, and chemokine receptors in lung tissue. Oak dust appeared to be a more potent inducer of these inflammatory mediators than birch dust. The results from our in vivo mouse model show that repeated airway exposure to wood dust can elicit lung inflammation, which is accompanied by induction of several proinflammatory cytokines and chemokines. Oak and birch dusts exhibited quantitative and qualitative differences in the elicitation of pulmonary inflammation, suggesting that the inflammatory responses induced by the wood species may rise via different cellular mechanisms.

The importance of fine particles has become apparent as the knowledge of their effects on health has increased. Fine particle concentrations have been published for outside air, plasma arc cutting, welding, and grinding, but little data exists for the woodworking industry. Sanding was evaluated as the producer of the woodworking industry's finest particles, and was selected as the target study. The number of dust particles in different particle size classes and the mass concentrations were measured in the following environments: workplace air during sanding in plywood production and in the inlet and return air; in the dust emission chamber; and in filter testing. The numbers of fine particles were low, less than 10(4) particles/cm(3) (10(7) particles/L). They were much lower than typical number concentrations near 10(6) particles/cm(3) measured in plasma arc cutting, grinding, and welding. Ultrafine particles in the size class less than 100 nm were found during sanding of MDF (medium density fiberboard) sheets. When the cleaned air is returned to the working areas, the dust content in extraction systems must be monitored continuously. One way to monitor the dust content in the return air is to use an after-filter and measure pressure drop across the filter to indicate leaks in the air-cleaning system. The best after-filtration materials provided a clear increase in pressure drop across the filter in the loading of the filter. The best after-filtration materials proved to be quite effective also for fine particles. The best mass removal efficiencies for fine particles around 0.3 mum were over 80% for some filter materials loaded with sanding wood dust.

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