The saimie paper suggests how susceptible individuals could reduce their total intake of aluminium. In presenting the cpidemiological evidence for a link betveen aluminium and Alzheimcr's, Nart'n suggests that although definite proof is still lacking, there is more than enough positixe evidence to fuel further epidemiological investigation. It states that such investigations might specificallx address the issue of the confounding cffect of silicon and an assessment of exposure to spccific

https://jech.bmj.com/content/jech/47/6/511.4.full.pdf

Methodology for Genetic Studies of Twins and Families

Background: Studies suggest that phthalate exposures may adversely affect child respiratory health.Objectives: We evaluated associations between asthma diagnosed in children between 5 and 11 years ...

/pdf/asthma-in-inner-city-children-at-5-11-years-of-age-and-1c240lyz88.pdf

Asthma in Inner-City Children at 5–11 Years of Age and Prenatal Exposure to Phthalates: The Columbia Center for Children’s Environmental Health Cohort

Background
Exhaled nitric oxide (FENO) measurements are used as a surrogate marker for eosinophilic airway inflammation. However, many constitutional and environmental factors affect FENO, making it difficult to devise reference values. Our aim was to evaluate the relative importance of factors affecting FENO in a well characterised adult population.

/pdf/factors-affecting-exhaled-nitric-oxide-measurements-the-2qdq4n5vll.pdf

Factors affecting exhaled nitric oxide measurements: the effect of sex

Background Factors affecting the fraction of nitric oxide in exhaled air (FE NO ) are multiple. Interpreting values when assessing airways disease may be problematic. Clinically optimum levels have not been defined. Objectives We aimed to establish the relationship between predicted values for FE NO obtained from equations by Olin et al, Travers et al, and Dressel et al, and normalized levels after oral prednisone. We also compared postprednisone FE NO levels with those obtained during optimized treatment with inhaled fluticasone. Methods Data were obtained before and after a trial of oral prednisone (30mg/d for 14 days), and also from a previously published study in which patients had their dose of inhaled corticosteroid adjusted using either FE NO or symptoms/lung function to optimize treatment. Results Seventy-three patients completed the study. The geometric mean FE NO after prednisone (17.7 parts per billion [ppb]; 95% CI, 15.5-20.2) was significantly lower than mean FE NO at the optimized fluticasone dose (20.2 ppb; 95% CI, 17.1-23.8; P =.04) and at loss of control (27.6 ppb; 95% CI, 22.8-33.4; P NO levels after prednisone did not differ significantly from the predicted values of Olin et al (16.8 ppb, 95% CI, 16.0-17.5; P =.44), but were significantly lower than values of Travers et al (predicted, 21.5 ppb; 95% CI, 20.9-22.2; P =.005) and Dressel et al (predicted, 27.8 ppb; 95% CI, 26.7-28.9; P Conclusions Optimum FE NO levels are best established by using oral rather than inhaled steroid treatment, and these approximate to predicted values from the reference equation by Olin et al. However, at optimized doses of inhaled corticosteroid, although FE NO levels were higher than predicted, asthma was well controlled. Targeting FE NO on reference values is not justified.

Exhaled nitric oxide levels in asthma: Personal best versus reference values.

Background Asthma is a significant cause of morbidity and mortality for African Americans. Fraction of exhaled nitric oxide (FeNO) levels are increased in patients with asthma, and airway levels of nitric oxide metabolites regulate airway inflammation and airway diameter. More needs to be known about the factors that regulate FeNO. There is a need for FeNO reference values for African Americans. Objective We sought to establish reference values and identify factors associated with FeNO levels in healthy African American adults. Methods FeNO levels were measured in 895 healthy, nonsmoking African Americans between the ages of 18 and 40 years. FeNO measurements were repeated in 84 subjects. Factors potentially associated with FeNO were measured, including blood pressure, height, weight, and serum total IgE, eosinophil cationic protein, C-reactive protein, and nitrate levels. Data on respiratory symptoms, including upper respiratory tract infection (URI) symptoms, were collected. Univariate and multivariate analyses of the relationship between these variables and FeNO levels were performed. Results In healthy, nonsmoking African Americans FeNO levels were stable during repeated measurements (intraclass correlation coefficient, 0.81). Sex ( P P P = .0002) contributed significantly to FeNO variability but together accounted for less than 50% of the variation in FeNO levels. Conclusion The high correlation between repeated measurements of FeNO and the low correlation coefficients of known factors associated with FeNO suggest that other factors might contribute substantially to variability of FeNO levels in African Americans.

Determinants of exhaled nitric oxide levels in healthy, nonsmoking African American adults.

Elevated levels of exhaled nitric oxide (eNO) and airway hyperresponsiveness are intermediate phenotypes of asthma. Using population-based data collected from a sample of twins, the present authors estimated the relative contribution of genes, family environment and nonshared environmental influences to variations in eNO and airway responsiveness (AR). In addition, the genetic and environmental sources of covariation between these two asthma-related phenotypes were investigated. The study population comprised a random sample of 377 adult twins identified through the Norwegian Twin Registry. The main outcome variables were eNO and AR to methacholine. Genetic effects accounted for 60% of the variation in eNO. Family environment accounted for 30% of the variation in AR, while nonshared environmental influences explained the remaining variation for both measures. For both eNO and AR, there were significant regression effects for atopy and smoking. The small, but significant association between eNO and AR was primarily explained by genetic factors. Sub-analyses restricted to atopic and nonsmoking twins strengthened the observation. In conclusion, variations in exhaled nitric oxide and airway responsiveness appear to be explained by different genetic and environmental variance structures. Variation in exhaled nitric oxide is explained by genetic and nonshared environmental effects, whereas an environmental model best explains the variation in airway responsiveness. Common genetic effects explain the small but significant association between exhaled nitric oxide and airway responsiveness.

https://erj.ersjournals.com/content/erj/29/2/292.full.pdf

Genetic and environmental effects on exhaled nitric oxide and airway responsiveness in a population-based sample of twins.

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Genetic and environmental effects on exhaled nitric oxide and airway responsiveness in a population-based sample of twins.