SMRs increased with cumulative arsenic exposure and with arsenic concentration ( Table 2 ). The SMR in the lowest concentration category was significantly elevated, suggesting a difference between respiratory cancer mortality rates for . males and a hypothetical group of nonexposed workers. We fitted model 1 with continuous cumulative arsenic exposure and six categories of arsenic concentration and estimated respiratory cancer rates in a hypothetical group of nonexposed workers relative to the standard population. After adjustment for arsenic exposure, SMRs for nonexposed workers were (95% CI, –), (95% CI, –), and (95% CI, –) for calendar periods < 1960, 1960–69, and ≥1970, respectively, and the effect of . birth relative to foreign birth was (95% CI, –). SMRs did not vary significantly with attained age. We included offset parameters fixed at the logarithms of these “nonexposed” SMRs to adjust for differences between “nonexposed” workers and the standard population. After adjustment, SMRs increased with cumulative arsenic exposure and with arsenic concentration, but at a lesser rate of increase ( Table 2 ).
The growth of children and adolescents receiving orally inhaled corticosteroids, including QVAR, should be monitored routinely (., via stadiometry). If a child or adolescent on any corticosteroid appears to have growth suppression, the possibility that he/she is particularly sensitive to this effect should be considered. The potential growth effects of prolonged treatment should be weighed against clinical benefits obtained and the risks associated with alternative therapies. To minimize the systemic effects of orally inhaled corticosteroids, including QVAR, each patient should be titrated to his/her lowest effective dose [see Dosage and Administration ( )] .
In this prospective, double-blind, placebo-controlled clinical trial, we randomized patients with COPD (FEV1 < 50% predicted plus at least one hospitalization due to exacerbation in the previous year) to ICS plus theophylline 100 mg bid or matched placebo. We determined the following at baseline and at the end of 52 weeks of follow-up: (1) HDAC activity in blood monocytes and sputum macrophages, (2) the concentration of several inflammatory markers (IL-8, IL-6, IL-1β, and tumor necrosis factor -α) in serum and sputum supernatant, and (3) the rates of exacerbations and adverse effects.