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How are asthmatics included in the derivation of guideline values for emergency planning and response?

How are asthmatics included in the derivation of guideline values for emergency planning and response?

Regul Toxicol Pharmacol. 2012 Jun 6;

Authors: Johansson MK, Johanson G, Oberg M

Abstract
Guideline values for emergency planning and response are aimed to protect the general public, including asthmatics and other susceptible groups, during sudden airborne releases of chemicals. A precondition of asthma may increase the individual susceptibility to acute exposures. This paper studies to what extent experimental data on asthmatics are included in the rationale and derivation of guideline values. An analysis of the Technical Support Documents (TSDs) of the Acute Exposure Guideline Levels (AEGL) shows that only 23 of the 176 TSDs include references to experimental studies on asthmatics, 30 include a statement on asthmatics but no reference to experimental data, and 123 lack any explicit statement on asthmatics. The TSDs were further compared with the support documents of nine other programs for acute or occupational short-term values. All programs were incomplete with respect to experimental data on asthmatics. Omission of asthmatics may interfere with trustful and efficient health protective actions. We suggest that the availability of data on asthmatics should be carefully examined in the development of guideline values, and that the lack of such data should be explicitly noted. In the latter case, available data for other irritants may be used to justify an appropriate assessment factor.

PMID: 22683397 [PubMed - as supplied by publisher]

Increased health risks of children with single mothers: the impact of socio-economic and environmental factors.

Increased health risks of children with single mothers: the impact of socio-economic and environmental factors.

Eur J Public Health. 2012 Jun 8;

Authors: Scharte M, Bolte G,

Abstract
BACKGROUND: Adverse effects of single parenthood on children's health have been reported before. Socio-economic difficulties are discussed as mediating factors. As child health also depends on environmental conditions, we investigated the impact of environmental exposures and socio-economic factors on differences in health outcomes of children with single mothers vs. couple families. METHODS: Data on 17 218 pre-school children (47% female) from three cross-sectional surveys conducted during 2004-07 in Germany were analysed. Health and exposure assessment were primarily based on parental report. Effects of socio-economic indicators (maternal education, household income) and environmental factors (traffic load at the place of residence, perceived environmental quality) on associations of four health outcomes (parent-reported health status, asthma, overweight, psychological problems) with single parenthood were determined by logistic regression analyses. RESULTS: Children with single mothers showed an increased risk regarding parent-reported poor health status [boys: odds ratio (OR) 1.39 (95% confidence interval (CI): 1.06-1.82), girls: 1.73 (1.28-2.33)], psychological problems [boys: 1.90 (1.38-2.61), girls: 1.58 (1.03-2.42)], overweight [only boys: OR 1.23 (1.01-1.50) and asthma [only girls: OR 1.90 (1.15-3.15)]. Adjusting for socio-economic factors attenuated the strength of the association of family type with child health. Although environmental factors were associated with most health outcomes investigated and children of single mothers were more often exposed, these environmental factors did not alter the differences between children with single mothers and couple families. CONCLUSIONS: The increased health risks of children from single-mother families vs. couple families are partly explained by socio-economic factors, but not by the environmental exposures studied.

PMID: 22683774 [PubMed - as supplied by publisher]

Glucocorticosteroids and β2-adrenoceptor agonists synergize to inhibit airway smooth muscle remodelling.

Airway remodelling, including increased airway smooth muscle (ASM) mass and contractility, contributes to increased airway narrowing in asthma. Increased ASM mass may be caused by exposure to mitogens, including platelet-derived growth factor (PDGF) and collagen type I, which induce a proliferative, hypocontractile ASM phenotype. By contrast, prolonged exposure to insulin induces a hypercontractile phenotype.

Glucocorticosteroids and β(2)-adrenoceptor agonists synergize to increase glucocorticosteroid receptor translocation in ASM cells; however, the impact of this synergism on phenotype modulation is unknown.

Using bovine tracheal smooth muscle, we investigated the effects of the glucocorticosteroids fluticasone (10 nM), budesonide (30 nM), dexamethasone (0.1-1 μM) and the combination of low concentrations of fluticasone (3-100 pM) and fenoterol (10 nM) on ASM phenotype switching in response to PDGF (10 ng/ml), collagen type I (50 μg/ml) and insulin (1 μM). All glucocorticosteroids inhibited PDGF- and collagen I-induced proliferation and hypocontractility, the effects of collagen I being less susceptible to glucocorticosteroid action. At 100-fold lower concentrations, fluticasone (100 pM) synergized with fenoterol to prevent PDGF- and collagen I-induced phenotype switching. This inhibition of ASM phenotype switching was associated with a normalization of the PDGF-induced decrease in the cell cycle inhibitors p21(WAF1/CIP1) and p57(KIP2). At this concentration, fluticasone also prevented the insulin-induced hypercontractile phenotype. At even lower concentrations, fluticasone (3 pM) synergized with fenoterol to inhibit this phenotype switch.

Collectively, these findings indicate that glucocorticosteroids and β(2)-agonists synergistically inhibit ASM phenotype switching, which may contribute to the increased effectiveness of combined treatment with glucocorticosteroids and β(2)-agonists in asthma.

Influence of socioeconomic status trajectories on innate immune responsiveness in children.

Lower socioeconomic status (SES) is consistently associated with poor health, yet little is known about the biological mechanisms underlying this inequality. In children, we examined the impact of early-life SES trajectories on the intensity of global innate immune activation, recognizing that excessive activation can be a precursor to inflammation and chronic disease.

METHODS: Stimulated interleukin-6 production, a measure of immune responsiveness, was analyzed ex vivo for 267 Canadian schoolchildren from a 1995 birth cohort in Manitoba, Canada. Childhood SES trajectories were determined from parent-reported housing data using a longitudinal latent-class modeling technique. Multivariate regression was conducted with adjustment for potential confounders.

RESULTS: SES was inversely associated with innate immune responsiveness (p = 0.003), with persistently low-SES children exhibiting responses more than twice as intense as their high-SES counterparts. Despite initially lower SES, responses from children experiencing increasing SES trajectories throughout childhood were indistinguishable from high-SES children. Low-SES effects were strongest among overweight children (p<0.01). Independent of SES trajectories, immune responsiveness was increased in First Nations children (p<0.05) and urban children with atopic asthma (p<0.01).

CONCLUSIONS: These results implicate differential immune activation in the association between SES and clinical outcomes, and broadly imply that SES interventions during childhood could limit or reverse the damaging biological effects of exposure to poverty during the preschool years.

Obesity in asthma: more neutrophilic inflammation as a possible explanation for a reduced treatment response.

The incidence of asthma and obesity is increasing worldwide, and reports suggest that obese patients have more severe asthma. We investigated whether obese asthma patients have more severe airway obstruction and airway hyper-responsiveness and a different type of airway inflammation than lean asthmatics. Furthermore, we assessed the effect of obesity on corticosteroid treatment response.

METHODS: Patient data from four well-documented asthma cohorts were pooled (n = 423). We evaluated FEV(1) , bronchial hyper-responsiveness (PC(20) ) to either methacholine/histamine or adenosine 5'-monophosphate (AMP) (differential) cell counts in induced sputum and blood and corticosteroid treatment response in 118 patients.

RESULTS: At baseline, FEV(1) , PC(20) methacholine or histamine, and PC(20) AMP values were comparable in 63 obese (BMI ≥30 kg/m(2) ) and 213 lean patients (BMI <25 kg/m(2) ). Obese patients had significantly higher blood neutrophils. These higher blood neutrophils were only seen in obese women and not in obese men. After a two-week treatment with corticosteroids, we observed less corticosteroid-induced improvement in FEV(1) %predicted in obese patients than in lean patients (median 1.7% vs 6.3% respectively, P = 0.04). The percentage of sputum eosinophils improved significantly less with higher BMI (P = 0.03), and the number of blood neutrophils increased less in obese than in lean patients (0.32 x10(3) /μl vs 0.57 x10(3) /μl, P = 0.046).

CONCLUSIONS: We found no differences in asthma severity between obese and nonobese asthmatics. Interestingly, obese patients demonstrated more neutrophils in sputum and blood than nonobese patients. The smaller improvement in FEV(1) and sputum eosinophils suggests a worse corticosteroid treatment response in obese asthmatics.

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