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For a given TPM level, the lung-delivered PM dose of sidestream CS was approximately two times higher than for mainstream CS (see Table 2).
The PM dose of asthmatics was influenced by the individual characteristics of the children, such as the inhalation rate, body weight and biological vulnerability.
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Cells were treated either with low (40 pM) or high (500 pM) doses of CLγ1 for 1 h and post-incubated in drug-free medium for 6 to 24 h.
The range of sensitivity among persons is uncertain because variations in PM exposure, PM dose, and host-related factors can cause exposed people to be more susceptible.
PM exposure dose of 1 μg/mL in the 6-well plates (growth area ∼10 cm) at the total volume of 1 mL corresponds to the surface area dose of 0.1 μg/cm.
Because the concentration of the weekly PM doses were the same for the 8-week PM-LD group and 16-week PM-HD groups, we were able to determine the progression of effects with repeated PM exposures.
The significant increase in the concentration of CRP, Hp, SAA and Pig-MAP have been also found previously in pigs infected with Pm only (the same strain and similar dose of Pm was used) [ 3].
However, the internal dose of PM also depends on breathing patterns and airway deposition, and cardiovascular and other systemic effects of PM require further translocation of PM constituents or signaling molecules or cells from the airways (Mills et al. 2009).
Table 1 shows the actual dose of PM inhaled by each person, taking ventilation into account.
Thus, the pulmonary dose of PM cannot account for the inhibited inflammatory response in the sidestream CS model.
The recommended dose of PM to achieve an ≈100% mortality rate is 1,000 mg/m² (29, 33 ), 6-fold the dosage that we used in our mixtures.
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