In general, endotoxin levels in the dust depend on a number of factors, such as the nature of the dust, land of origin of the product, conditions during transport, the particle size during processing, temperature, and humidity. For the workers, particle size seems to be the most important factor involved in the endotoxin/ dust ratio. In general, large dust particles will contain relatively small ratios of endotoxin whereas small dust particles will contain a relatively large ratio of endotoxin. No measurements of dust or endotoxin were performed in the office environment. However, a possible exposure of the office workers to endotoxin only tends to reduce the reported significance between our exposed and control group.
From our data it is difficult to conclude if endotoxin is a causal factor and whether effects are short or long term. Castellan et al showed that endotoxin might be a causal factor in an exposure system. In the absence of a correlation between concentrations of cotton dust and endotoxin (r=0.07; p=0.46), they found no correlation of the cotton dust concentration with the group mean percentage change in FEVi in subjects exposed this inhalers for asthma. In contrast a clear exposure response was observed between endotoxin and group mean percentage change in FEVi. They suggested that measuring the endotoxin concentration in air is a much more reliable means of assessing the risk of an acute airway response to cotton dust than measuring the mass concentration of dust. In our study among animal feed processors, a significant correlation coefficient of airborne dust with endotoxin (r=0.81; p<0.01) was observed. This means that it is difficult to subscribe effects measured to either airborne dust or endotoxin. However in a similar study, Smid et al showed a higher correlation between cumulative endotoxin exposure and all flow volume parameters studied than between dust and lung function decrements.