Relationships between socioeconomic and lifestyle factors and indoor air quality in French dwellings.

BACKGROUND: To date, few studies have analyzed the relationships between socioeconomic status (SES) and indoor air quality (IAQ). OBJECTIVE: The aim of this study was to examine the relationships between socioeconomic and other factors and indoor air pollutant levels in French homes. METHODS: The indoor air concentrations of thirty chemical, biological and physical parameters were measured over one week in a sample of 567 dwellings representative of the French housing stock between September 2003 and December 2005. Information on SES (household structure, educational attainment, income, and occupation), building characteristics, and occupants' habits and activities (smoking, cooking, cleaning, etc.) were collected through administered questionnaires. Separate stepwise linear regression models were fitted to log-transformed concentrations on SES and other factors. Logistic regression was performed on fungal contamination data. RESULTS: Households with lower income were more likely to have higher indoor concentrations of formaldehyde, but lower perchloroethylene indoor concentrations. Formaldehyde indoor concentrations were also associated with newly built buildings. Smoking was associated with increasing acetaldehyde and PM2.5 levels and the risk of a positive fungal contamination index. BTEX levels were also associated with occupant density and having an attached garage. The major predictors for fungal contamination were dampness and absolute humidity. CONCLUSION: These results, obtained from a large sample of dwellings, show for the first time in France the relationships between SES factors and indoor air pollutants, and believe they should be considered alongside occupant activities and building characteristics when study IAQ in homes.

Quantitative assessments of indoor air pollution and respiratory health in a population-based sample of French dwellings.

BACKGROUND: Various volatile organic compounds (VOCs) have been related to respiratory health effects, but have generally been assessed individually without taking into account the fact that such pollutants are highly correlated to one other. AIMS: We investigated the effects of exposure to various VOC, and considered their combined effect on adult asthma and rhinitis. METHOD: A national cross-sectional representative survey conducted by the Indoor Air Quality Observatory objectively assessed 20 VOCs in 490 main dwellings in France. A standardized questionnaire determined the prevalence of asthma and rhinitis among 1012 inhabitants of the dwellings (≥ 15 years). Marginal models for binary outcome were used to relate VOCs exposure to asthma and rhinitis, controlling for potential confounders. A global score representing the number of VOCs in each dwelling with an elevated concentration (using the 3(rd) quartile value of the distribution as a threshold value) was then derived as a measure of the combined effect of VOCs. Specific scores were built using a similar approach, grouping VOCs by family. RESULTS: Asthma (8.6%) was significantly associated with N-undecane and 1,2,4-trimethylbenzene and rhinitis (38.3%) with ethylbenzene, trichloroethylene, m/p- and o-xylene. The global VOC score was associated with a significant risk of asthma and rhinitis (odds ratio (OR) of 1.40 and 1.22, respectively, for 5 additional VOCs with high exposure level). Both specific scores for aromatic hydrocarbons and aliphatic hydrocarbons were associated with a significantly risk of asthma (OR=1.12; 95% confidence interval (CI): 1.01-1.24 and OR=1.41; 95% CI=1.03-1.93, respectively). The specific VOC score for halogenated hydrocarbons was associated with a significant risk of rhinitis (OR=1.28; 95% CI: 1.07-1.54). CONCLUSION: We have shown that high concentrations of VOCs in homes were associated with an increasing prevalence of asthma and rhinitis in adults.

Socio-economic costs of indoor air pollution: A tentative estimation for some pollutants of health interest in France.

An evaluation of the socio-economic costs of indoor air pollution can facilitate the development of appropriate public policies. For the first time in France, such an evaluation was conducted for six selected pollutants: benzene, trichloroethylene, radon, carbon monoxide, particles (PM2.5 fraction), and environmental tobacco smoke (ETS). The health impacts of indoor exposure were either already available in published works or were calculated. For these calculations, two approaches were followed depending on the available data: the first followed the principles of quantitative health risk assessment, and the second was based on concepts and methods related to the health impact assessment. For both approaches, toxicological data and indoor concentrations related to each target pollutant were used. External costs resulting from mortality, morbidity (life quality loss) and production losses attributable to these health impacts were assessed. In addition, the monetary costs for the public were determined. Indoor pollution associated with the selected pollutants was estimated to have cost approximately €20 billion in France in 2004. Particles contributed the most to the total cost (75%), followed by radon. Premature death and the costs of the quality of life loss accounted for approximately 90% of the total cost. Despite the use of different methods and data, similar evaluations previously conducted in other countries yielded figures within the same order of magnitude.

Higher prevalence of breathlessness in elderly exposed to indoor aldehydes and VOCs in a representative sample of French dwellings.

The purpose of this study was to explore respiratory health effects of indoor exposures to aldehydes and volatile organic compounds (VOCs) in elderly living in a population-based representative sample of French dwellings and to compare them to the rest of the occupants of the dwellings. Twenty VOCs were objectively measured in 490 main dwellings. The respiratory conditions were assessed through a standardized questionnaire in 1012 inhabitants aged over 15 years, 144 of whom were aged over 65 years. Generalized estimating equations (GEE) were used to model the relationship between respiratory health outcomes and air pollutants concentrations using the median value of the distribution to define elevated exposure. Similar levels of indoor air pollutants were found in elderly and others. However, associations between breathlessness and living in dwellings with elevated concentrations of toluene and o-xylene respectively were statistically significant in elderly but not in the rest of the population (adjusted odds ratios (AOR(95% confidence interval) = 3.36(1.13, 9.98) and 2.85(1.06, 7.68) in elderly vs. 0.91(0.59, 1.39) and 0.79( 0.47, 1.34) in the others respectively). A more pronounced effect of n-decane on past year breathlessness was observed in case of poor ventilation in the dwellings. Our results showed a higher risk of breathlessness in elderly exposed to indoor air pollution than in the rest of the exposed population. Further investigations are needed to confirm whether this is related to frailty in elderly.

Bisphenol A diglycidyl ether induces adipogenic differentiation of multipotent stromal stem cells through a peroxisome proliferator-activated receptor gamma-independent mechanism.

BACKGROUND: Bisphenol A (BPA) and bisphenol A diglycidyl ether (BADGE), used in manufacturing coatings and resins, leach from packaging materials into food. Numerous studies suggested that BPA and BADGE may have adverse effects on human health, including the possibility that exposure to such chemicals can be superimposed on traditional risk factors to initiate or exacerbate the development of obesity. BPA is a suspected obesogen, whereas BADGE, described as a peroxisome proliferator-activated receptor gamma (PPARγ) antagonist, could reduce weight gain. OBJECTIVES: We sought to test the adipogenic effects of BADGE in a biologically relevant cell culture model. METHODS: We used multipotent mesenchymal stromal stem cells (MSCs) to study the adipogenic capacity of BADGE and BPA and evaluated their effects on adipogenesis, osteogenesis, gene expression, and nuclear receptor activation. DISCUSSION: BADGE induced adipogenesis in human and mouse MSCs, as well as in mouse 3T3-L1 preadipocytes. In contrast, BPA failed to promote adipogenesis in MSCs, but induced adipogenesis in 3T3-L1 cells. BADGE exposure elicited an adipogenic gene expression profile, and its ability to induce adipogenesis and the expression of adipogenic genes was not blocked by known PPARγ antagonists. Neither BADGE nor BPA activated or antagonized retinoid "X" receptor (RXR) or PPARγ in transient transfection assays. CONCLUSIONS: BADGE can induce adipogenic differentiation in both MSCs and in preadipocytes at low nanomolar concentrations comparable to those that have been observed in limited human biomonitoring. BADGE probably acts through a mechanism that is downstream of, or parallel to, PPARγ.

Prenatal exposure to the environmental obesogen tributyltin predisposes multipotent stem cells to become adipocytes.

The environmental obesogen hypothesis proposes that pre- and postnatal exposure to environmental chemicals contributes to adipogenesis and the development of obesity. Tributyltin (TBT) is an agonist of both retinoid X receptor (RXR) and peroxisome proliferator-activated receptor gamma (PPARgamma). Activation of these receptors can elevate adipose mass in adult mice exposed to the chemical in utero. Here we show that TBT sensitizes human and mouse multipotent stromal stem cells derived from white adipose tissue [adipose-derived stromal stem cells (ADSCs)] to undergo adipogenesis. In vitro exposure to TBT, or the PPARgamma activator rosiglitazone increases adipogenesis, cellular lipid content, and expression of adipogenic genes. The adipogenic effects of TBT and rosiglitazone were blocked by the addition of PPARgamma antagonists, suggesting that activation of PPARgamma mediates the effect of both compounds on adipogenesis. ADSCs from mice exposed to TBT in utero showed increased adipogenic capacity and reduced osteogenic capacity with enhanced lipid accumulation in response to adipogenic induction. ADSCs retrieved from animals exposed to TBT in utero showed increased expression of PPARgamma target genes such as the early adipogenic differentiation gene marker fatty acid-binding protein 4 and hypomethylation of the promoter/enhancer region of the fatty acid-binding protein 4 locus. Hence, TBT alters the stem cell compartment by sensitizing multipotent stromal stem cells to differentiate into adipocytes, an effect that could likely increase adipose mass over time.

Pregnane X receptor knockout mice display osteopenia with reduced bone formation and enhanced bone resorption.

The steroid and xenobiotic receptor (SXR) and its murine ortholog pregnane X receptor (PXR) are nuclear receptors that are expressed mainly in the liver and intestine where they function as xenobiotic sensors. In addition to its role as a xenobiotic sensor, previous studies in our laboratories and elsewhere have identified a role for SXR/PXR as a mediator of bone homeostasis. Here, we report that systemic deletion of PXR results in marked osteopenia with mechanical fragility in female mice as young as 4 months old. Bone mineral density (BMD) of PXR knockout (PXRKO) mice was significantly decreased compared with the BMD of wild-type (WT) mice. Micro-computed tomography analysis of femoral trabecular bones revealed that the three-dimensional bone volume fraction of PXRKO mice was markedly reduced compared with that of WT mice. Histomorphometrical analysis of the trabecular bones in the proximal tibia showed a remarkable reduction in bone mass in PXRKO mice. As for bone turnover of the trabecular bones, bone formation is reduced, whereas bone resorption is enhanced in PXRKO mice. Histomorphometrical analysis of femoral cortical bones revealed a larger cortical area in WT mice than that in PXRKO mice. WT mice had a thicker cortical width than PXRKO mice. Three-point bending test revealed that these morphological phenotypes actually caused mechanical fragility. Lastly, serum levels of phosphate, calcium, and alkaline phosphatase were unchanged in PXRKO mice compared with WT. Consistent with our previous results, we conclude that SXR/PXR promotes bone formation and suppresses bone resorption thus cementing a role for SXR/PXR as a key regulator of bone homeostasis.

The role of hepatic, renal and intestinal gluconeogenic enzymes in glucose homeostasis of juvenile rainbow trout.

Rainbow trout is unable to utilize high levels of dietary carbohydrates and experiences hyperglycemia after consumption of carbohydrate-rich meals. Carbohydrates stimulate hepatic glycolytic activity, but gene expression of the rate-limiting gluconeogenic enzymes glucose-6-phosphatase (G6Pase), fructose-1,6-bisphosphatase (FBPase) and phosphoenolpyruvate carboxykinase (PEPCK) remains high. Although there is significant mRNA expression and activity of gluconeogenic enzymes in trout intestine and kidney, the regulation of these enzymes by diet is not known. We tested the hypothesis that dietary carbohydrate modulates intestinal and renal G6Pase, FBPase and PEPCK. Fish were either fasted or fed isocaloric carbohydrate-free (CF) or high carbohydrate (HC) diets for 14 days. As expected, fish fed HC exhibited postprandial hyperglycemia and enhanced levels of hepatic glucokinase mRNA and activity. Dietary carbohydrates had no significant effect on the expression and activity of PEPCK, FBPase and G6Pase in all three organs. In contrast, fasting enhanced the activity, but not the mRNA expression of both hepatic and intestinal PEPCK, as well as intestinal FBPase. Therefore, the activity of rate-limiting gluconeogenic enzymes in trout can be modified by fasting, but not by the carbohydrate content of the diet, potentially causing hyperglycemia when fed high levels of dietary carbohydrates. In this species consuming low carbohydrate diets at infrequent intervals in the wild, fasting-induced increases in hepatic and intestinal gluconeogenic enzyme activities may be a key adaptation to prevent perturbations in blood glucose during food deprivation.

Luminal fructose inhibits rat intestinal sodium-phosphate cotransporter gene expression and phosphate uptake.

BACKGROUND: While searching by microarray for sugar-responsive genes, we inadvertently discovered that sodium-phosphate cotransporter 2B (NaPi-2b) mRNA concentrations were much lower in fructose-perfused than in glucose-perfused intestines of neonatal rats. Changes in NaPi-2b mRNA abundance by sugars were accompanied by similar changes in NaPi-2b protein abundance and in rates of inorganic phosphate (Pi) uptake. OBJECTIVE: We tested the hypothesis that luminal fructose regulates NaPi-2b. DESIGN: We perfused into the intestine fructose, glucose, and nonmetabolizable or poorly transported glucose analogs as well as phlorizin. RESULTS: NaPi-2b mRNA concentrations and Pi uptake rates in fructose-perfused intestines were approximately 30% of those in glucose and its analogs. NaPi-2b inhibition by fructose is specific because the mRNA abundance and activity of the fructose transporter GLUT5 (glucose transporter 5) increased with fructose perfusion, whereas those of other transporters were independent of the perfusate. Plasma Pi after 4 h of perfusion was independent of the perfusate, probably because normal kidneys can maintain normophosphatemia. Inhibiting glucose-6-phosphatase, another fructose-responsive gene, with tungstate or vanadate nonspecifically inhibited NaPi-2b mRNA expression and Pi uptake in both glucose- or fructose-perfused intestines. The AMP kinase (AMPK)-activator AICAR (5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside) enhanced and the fatty acid synthase-AMPK inhibitor C75 (3-carboxy-4-octyl-2-methylenebutyrolactone trans-4-carboxy-5-octyl-3-methylenebutyrolactone) prevented fructose inhibition of NaPi-2b but had no effect on expression of other transporters. NaPi-2b expression decreased markedly with age and was inhibited by fructose in all age groups. CONCLUSIONS: Energy levels in enterocytes may play a role in NaPi-2b inhibition by luminal fructose. Consumption of fructose that supplies approximately 10% of caloric intake by Americans clearly affects absorption of Pi and may promote Pi homeostasis in patients with impaired renal function.

Vanadate but not tungstate prevents the fructose-induced increase in GLUT5 expression and fructose uptake by neonatal rat intestine.

Intermediary signals, precociously enhancing GLUT5 transcription in response to perfusion of its substrate, fructose, in the small intestine of neonatal rats, are not known. Because glucose-6-phosphatase (G6Pase), glucose-6-phosphate translocase (G6PT), and fructose-1,6-bisphosphatase (FBPase) expression increases parallel to or precedes that of GLUT5, we investigated the link between these gluconeogenic genes and GLUT5 by using vanadate or tungstate, potent inhibitors of gluconeogenesis. Small intestinal perfusions of 20-d-old rats were performed with fructose alone, fructose + vanadate or tungstate, glucose alone, and glucose + vanadate or tungstate. As expected, fructose, but not glucose nor glucose + inhibitor perfusion, increased GLUT5 mRNA abundance and fructose transport. Fructose perfusion dramatically increased G6Pase mRNA abundance but had no effect on G6Pase activity. In sharp contrast, fructose perfusion did not increase FBPase gene expression but stimulated FBPase activity. Both vanadate and tungstate significantly inhibited G6Pase activity but did not prevent the fructose-induced increases in G6Pase and G6PT gene expression. Perfusion with fructose + vanadate prevented the fructose-induced increases in fructose transport and GLUT5 mRNA abundance, whereas perfusion with fructose + tungstate did not. Interestingly, vanadate, but not tungstate, inhibited the fructose-induced increase in FBPase activity. Thus, vanadate inhibition of fructose-induced increases in FBPase activity paralleled exactly vanadate inhibition of fructose-induced increases in GLUT5 mRNA abundance and activity. Fructose-induced changes in FBPase activity may regulate changes in GLUT5 expression and activity in the small intestine of neonatal rats. The marked increases in intestinal G6Pase and GLUT5 mRNA abundance may be a parallel response to different factors released during fructose perfusion.

Dependence on sampling rates of Radiello((R)) diffusion sampler for BTEX measurements with the concentration level and exposure time.

Radiello((R)) diffusive samplers filled with a thermally desorbable adsorbent (graphitised charcoal Carbograph 4) have been tested for the monitoring of BTEX. The sampling rates have been estimated under various controlled atmospheres in order to evaluate the effects of two factors (exposure time, concentration levels and their interaction) on the performances of the Radiello((R)) sampler. Experiments have been carried out under various atmospheres in exposure chamber. A total of 174 Radiello((R)) samplers were exposed while varying two conditions: exposure time (1, 3, 7 and 14 days) and BTEX concentrations (low, medium and high levels). The results show that the sampling rates of benzene and toluene decrease for exposure of 14 days and especially for high concentration levels: decrease of 30% at 10mugm(-3) for benzene and 14% at 30mugm(-3) for toluene. To try to explain the variations of these sampling rates, the breakthrough volumes (V(B)) of BTEX on Carbograph 4 have been determined at different temperature and concentration conditions in order to evaluate the Langmuir parameters and their adsorption enthalpy (-DeltaH(ads)) using the Van't Hoff equation. With regard to these adsorption characteristics, the dependence of sampling rates with concentration level and exposure time were analysed and discussed.

Low protein intake is associated with reduced hepatic gluconeogenic enzyme expression in rainbow trout (Oncorhynchus mykiss).

Our objective was to understand the reasons behind the persistent postprandial hyperglycemia in rainbow trout (Oncorhynchus mykiss). We hypothesized that in this species, high levels of dietary protein could increase the hepatic production of glucose, irrespective of the dietary carbohydrate supply. We fed juvenile rainbow trout four diets containing graded levels of protein for 14 d. Pair-feeding was employed to keep lipid and carbohydrate intakes constant. Six hours after feeding, as postulated, activities and mRNA levels of gluconeogenic enzymes (glucose-6-phosphatase, fructose-1,6-bisphosphatase) increased with increasing dietary protein (P < 0.05). However, in fish with a very low protein intake, there was a very strong increase in plasma glucose (18 mmol/L) that was also associated with a high capacity to store excess glucose as indicated by altered pyruvate kinase activity, glucokinase activity, and hepatic glycogen and fat concentrations (P < 0.05). In conclusion, at the same level of carbohydrate intake, a low dietary protein intake was associated with an unexplained increase in glycemia, which was probably responsible for the decrease in hepatic gluconeogenic enzyme expression. The effect of dietary protein on low carbohydrate utilization in this species remains unclear.