Bronchial Reactivity, Inflammatory and Allergic Parameters, and Vitamin D Levels in Children With Asthma.

BACKGROUND: A low serum vitamin D level may represent a marker of other perplexing factors that may lead to increased asthma prevalence and severity. Our aim was to assess the correlation between vitamin D levels and asthma and allergy markers in a subgroup of children with fewer confounding factors. METHODS: Non-obese children (6-18 y old) with asthma who were not receiving anti-inflammatory treatment were recruited. Subjects underwent spirometry with a methacholine challenge test, and fractional exhaled nitric oxide (FENO), serum vitamin D levels, total immunoglobulin E (IgE) levels, blood eosinophil counts, and high-sensitivity C-reactive protein levels were determined. The primary end point was the correlation between vitamin D level and airway hyper-responsiveness as assessed by a methacholine challenge test. The secondary end point was the correlation between vitamin D level and FENO, systemic inflammatory markers, and allergy. RESULTS: Seventy-one children with asthma (25 females, 35%; 12.5 ± 3.6 y of age) were included. The median vitamin D level was 23 ng/mL (range of 6-48.5, mean of 23.02 ± 7.74), the median IgE level was 305 IU/mL (range of 4.3-4,240), the median provocational concentration of methacholine that produced a 20% decrease in FEV1 was 1.1 mg/mL (range of 0-13.9), and the median FENO was 26.5 ppb (range of 3.6-285). No correlation was found between vitamin D level and response to the methacholine challenge test, FENO, high-sensitivity C-reactive protein levels, IgE levels, eosinophil counts, and frequency of allergic rhinitis or atopic dermatitis. CONCLUSIONS: In our group of children with asthma, no correlation was found between the level of vitamin D and the degree of airway reactivity, airway inflammation, and allergy. The cause-and-effect relationship between vitamin D, asthma, and allergy should be further clarified. (ClinicalTrials.gov registration NCT01287455).

Dose-response assessment and effect of particles in guinea pigs exposed chronically to diesel exhaust: analysis of various biological markers in pulmonary alveolar lavage fluid and circulating blood.

To elucidate dose-response and other effects of diesel particles in guinea pigs chronically exposed to diesel exhaust, various biomarkers for chronic obstructive lung diseases were studied using bronchoalveolar lavage (BAL) fluid and blood specimens. Guinea pigs were exposed 16 h/day, 6 days/wk, for 6, 12, 18, or 24 mo to filtered air (control group, n = 8-10), a low level of diesel exhaust (L group: NO(2) = 0.22 +/- 0.03 ppm; SO(2) = 0.6 +/- 0.19 ppm; particles = 0.21 +/- 0.07 mg/m(3), n = 8-10), medium level of diesel exhaust (M group; NO(2) = 1.07 +/- 0.09 ppm; SO(2) = 2.83 +/- 0.73 ppm; particles = 1.14 +/- 0.26 mg/m(3), n = 8-10), and high level of diesel exhaust (H group: NO(2) = 2.88 +/- 0.29 ppm; SO(2) = 6.49 +/- 1.75 ppm; particles = 2.94 +/- 0.69 mg/m(3), n = 8-10), or at a medium concentration of diesel exhaust without particulate matters (MG group: NO(2) = 1.01 +/- 0.09 ppm;#10; SO(2) = 2.66 +/- 0.64 ppm; particles = 0.01 +/- 0.01 mg/m(3), n = 8-10). Anesthetized animals were sacrificed and BAL fluid from the lung and blood from right ventricle were collected. Various biomarkers of inflammation, components of mucus and surfactant, bronchoconstrictors were determined. Changes of leukotriene C4 in plasma, eosinophil counts, biomarkers of inflammation and cytotoxicity, and mucus and surfactant components in BAL fluid were statistically different among the C, L, M, and H groups after adjustment for the exposure period and group-by-exposure period with respect to their interactions in two-way analysis of variance (ANOVA). The levels of these biomarkers in the H group were higher than those of the M group, whereas those of the L group showed no significant changes compared with those of the C group during experimental period. Onset of significant changes of these biomarkers for the M group was at 18 mo of exposure, whereas that for the H group was at 12 mo of exposure, which resulted in changes in the levels of biomarkers in BAL fluid. Although numbers of eosinophils in BAL fluid increased significantly in the M and H groups at 12 mo, only leukotriene C4 increased at 18 and 24 mo in blood and at 24 mo in BAL fluid. Animals exposed to the medium level of diesel exhaust without particulate matter showed significantly less increase of these biomarkers as compared with animals exposed to the same level of diesel exhaust with particulate matters. These findings indicate that chronic exposure to diesel exhaust induced continuous inflammation, overproduction of mucus, and phospholipids in the lung. Animals exposed to the high dose of diesel exhaust showed a plateau of biological responses at 12 mo of exposure. Particulate matter in diesel exhaust appears to play an important role in development of lung injury by chronic emission exhaust exposure.

Determination of methyltetrahydrophthalic anhydride in air using gas chromatography with electron-capture detection.

Methyltetrahydrophthalic anhydride (MTHPA) stimulates the production of specific IgE antibodies which can cause occupational allergy even at extremely low levels of exposure (15-22 micrograms/m3). Safe use in industry demands control of the levels of exposure causing allergic diseases. Thus, the air monitoring of MTHPA is very important, and sensitive methods are required to measure low air concentrations or short-time peak exposures. This paper outlines the use of silica-gel tubes for sampling airborne MTHPA vapour, followed by analysis using gas chromatography with electron-capture detection. No breakthrough was observed at 113, 217, 673 and 830 micrograms/m3 (sampling volume 30, 60, 60 and 20 l, respectively; relative humidity 40-55%). Concentrations > 1.0 microgram/m3 could be quantified at 20-min sampling with a sampling rate of 1 l/min. The present method can also be applied to measurements of exposure to hexahydrophthalic and methylhexahydrophthalic anhydride. The risk of MTHPA exposure in two condenser plants was also assessed by determining MTHPA levels in air of the workplace. In conclusion, our method was found to be reliable and sensitive, and can be applied to the evaluation of MTHPA exposure.