Pathogenesis.
The development of a pneumoconiosis depends on
(1) the amount of dust retained in the lung and airways; (2) the size, shape, and therefore buoyancy of the particles; (3) particle solubility and physiochemical reactivity; and (4) the possible additional effects of other irritants (e.g., concomitant tobacco smoking).
The amount of dust retained in the lungs is determined by the dust concentration in ambient air, the duration of exposure, and the effectiveness of clearance mechanisms. Any influence, such as cigarette smoking, that affects the integrity of the mucociliary apparatus significantly predisposes to the accumulation of dust.
The most dangerous particles range from 1 to 5 μm in diameter because they may reach the terminal small airways and air sacs and settle in their linings. Under normal conditions there is a small pool of intra-alveolar macrophages, and this is expanded by recruitment of more macrophages when dust reaches the alveolar spaces. The protection provided by phagocytosis of particles, however, can be overwhelmed by a large dust burden by specific chemical interactions of the particles with cells.
The solubility and cytotoxicity of particles, which are influenced to a considerable extent by their size, modify the nature of the pulmonary response. In general, the smaller the particle, the more likely it is to appear in the pulmonary fluids and reach toxic levels rapidly, depending, of course, on the solubility of the agent. Therefore, smaller particles tend to cause acute lung injury. Larger particles resist dissolution and so may persist within the lung parenchyma for years. These tend to evoke fibrosing collagenous pneumoconioses, such as is characteristic of silicosis. Some of the particles may be taken up by epithelial cells or may cross the epithelial cell lining and interact directly with fibroblasts and interstitial macrophages. Some may reach the lymphatics by direct drainage or within migrating macrophages and thereby initiate an immune response to components of the particulates or to self-proteins modified by the particles or both. This response amplifies the intensity and the duration of the local reaction. Although
tobacco smoking worsens the effects of all inhaled mineral dusts, the effects of asbestos are particularly magnified by smoking. The effects of inhaled particles are not confined to the lung alone, since solutes from particles can enter the blood and lung inflammation invokes systemic responses.
then I found out that I had the tank screwed together to tight. opened it up pulled off the little condom put it back on and lightly screwed the tank back together now its working no dry hits 
