Background The development of asthma after respiratory syncytial virus (RSV) bronchiolitis has been demonstrated in case-control studies, although the determinants of post-RSV asthma remain undefined. Objectives We sought to evaluate the potential determinants of physician-diagnosed asthma after severe RSV bronchiolitis during infancy. Methods We enrolled 206 children during an initial episode of severe RSV bronchiolitis at 12 months of age or less in a prospective cohort study and followed these children for up to 6 years. In a subset of 81 children, we analyzed CCL5 (RANTES) mRNA expression in upper airway epithelial cells. Results Forty-eight percent of children had physician-diagnosed asthma before the seventh birthday. Independent determinants significantly associated with increased risk for physician-diagnosed asthma by the seventh birthday included maternal asthma (odds ratio [OR], 5.2; 95% CI, 1.7-15.9; P = .004), exposure to high levels of dog allergen (OR, 3.2; 95% CI, 1.3-7.7; P = .012), aeroallergen sensitivity at age 3 years (OR, 10.7; 95% CI, 2.1-55.0; P = .005), recurrent wheezing during the first 3 years of life (OR, 7.3; 95% CI, 1.2-43.3; P = .028), and CCL5 expression in nasal epithelia during acute RSV infection (OR, 3.8; 95% CI, 1.2-2.4; P < .001). White children (OR, 0.19; 95% CI, 0.04-0.93; P = .041) and children attending day care (OR, 0.18; 95% CI, 0.04-0.84; P = .029) had a decreased risk of physician-diagnosed asthma. Conclusions Approximately 50% of children who experience severe RSV bronchiolitis have a subsequent asthma diagnosis. The presence of increased CCL5 levels in nasal epithelia at the time of bronchiolitis or the development of allergic sensitization by age 3 years are associated with increased likelihood of subsequent asthma.

Potential reproductive effects from occupational exposures to ethylene glycol ethers (EGE) are of concern since these organic solvents have been used widely in industry, and their reproductive toxicity has been well documented in animal studies. For determination of whether occupational exposure to EGE was associated with increased risks of spontaneous abortion and subfertility (i.e., taking more than 1 year of unprotected intercourse to conceive), a retrospective cohort study was conducted among workers at two semiconductor manufacturing plants in the eastern United States in 1980-1989 as part of a larger evaluation of reproductive health. Reproductive and occupational histories were obtained from interviews of semiconductor manufacturing workers and spouses. Assessment of potential exposure to mixtures containing EGE (none, low, medium, and high) was based on reported processes and company records. There were 1,150 pregnancies to semiconductor manufacturers, 561 to female employees and 589 to wives of male employees. Among female manufacturers, potential exposure to mixtures containing EGE was associated with increased risks of spontaneous abortion (relative risk in the high exposure group = 2.8; 95% confidence interval (CI) 1.4-5.6) and subfertility (odds ratio in the high exposure group = 4.6; 95% CI 1.6-13.3). Both of these risks exhibited a dose-response relation with potential EGE exposure (p for trend = 0.02). Among spouses of male manufacturers potentially exposed to mixtures containing EGE, there was no increased risk of spontaneous abortion, but there was a nonsignificant increased risk of subfertility (odds ratio in the high exposure group = 1.7; 95% CI 0.7-4.3).

Background Direct comparisons between SFAs varying in chain length, specifically palmitic acid (16:0) and stearic acid (18:0), relative to the latter's metabolic product, oleic acid (18:1), on cardiometabolic risk factors are limited. Objective The aim of this study was to determine the relative comparability of diets enriched in palmitic acid, stearic acid, and oleic acid on inflammation and coagulation markers, T lymphocyte proliferation/ex-vivo cytokine secretion, plasma cardiometabolic risk factors, and fecal bile acid concentrations. Methods Hypercholesterolemic postmenopausal women (n = 20, mean ± SD age 64 ± 7 y, BMI 26.4 ± 3.4 kg/m2, LDL cholesterol ≥ 2.8 mmol/L) were provided with each of 3 diets [55% energy (%E) carbohydrate, 15%E protein, 30%E fat, with ∼50% fat contributed by palmitic acid, stearic acid, or oleic acid in each diet; 5 wk/diet phase] using a randomized crossover design with 2-wk washouts between phases. Outcome measures were assessed at the end of each phase. Results Fasting LDL-cholesterol and non–HDL-cholesterol concentrations were lower after the stearic acid and oleic acid diets than the palmitic acid diet (all P &lt; 0.01). Fasting HDL-cholesterol concentrations were lower after the stearic acid diet than the palmitic acid and oleic acid diets (P &lt; 0.01). The stearic acid diet resulted in lower lithocholic acid (P = 0.01) and total secondary bile acid (SBA) concentrations (P = 0.04) than the oleic acid diet. All other outcome measures were similar between diets. Lithocholic acid concentrations were positively correlated with fasting LDL-cholesterol concentrations (r = 0.33; P = 0.011). Total SBA, lithocholic acid, and deoxycholic acid concentrations were negatively correlated with fasting HDL cholesterol (r = −0.51 to −0.44; P &lt; 0.01) concentrations and positively correlated with LDL cholesterol:HDL cholesterol (r = 0.37–0.54; P &lt; 0.01) ratios. Conclusions Dietary stearic acid and oleic acid had similar effects on fasting LDL-cholesterol and non–HDL-cholesterol concentrations and more favorable ones than palmitic acid. Unlike oleic acid, the hypocholesterolemic effect of stearic acid may be mediated by inhibition of intestinal hydrophobic SBA synthesis. These findings add to the data suggesting there should be a reassessment of current SFA dietary guidance and Nutrient Facts panel labeling. This trial was registered at clinicaltrials.gov as NCT02145936.

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