Association between consumption of nonessential energy-dense food and body mass index among Mexican school-aged children: a prospective cohort study.

BACKGROUND/OBJECTIVES: Obesity prevalence in Mexican children has increased rapidly and is among the highest in the world. We aimed to estimate the longitudinal association between nonessential energy-dense food (NEDF) consumption and body mass index (BMI) in school-aged children 5 to 11 years, using a cohort study with 6 years of follow-up. SUBJECTS/METHODS: We studied the offspring of women in the Prenatal omega-3 fatty acid supplementation, child growth, and development (POSGRAD) cohort study. NEDF was classified into four main groups: chips and popcorn, sweet bakery products, non-cereal based sweets, and ready-to-eat cereals. We fitted fixed effects models to assess the association between change in NEDF consumption and changes in BMI. RESULTS: Between 5 and 11 years, children increased their consumption of NEDF by 225 kJ/day (53.9 kcal/day). In fully adjusted models, we found that change in total NEDF was not associated with change in children's BMI (0.033 kg/m2, [p = 0.246]). However, BMI increased 0.078 kg/m2 for every 418.6 kJ/day (100 kcal/day) of sweet bakery products (p = 0.035) in fully adjusted models. For chips and popcorn, BMI increased 0.208 kg/m2 (p = 0.035), yet, the association was attenuated after adjustment (p = 0.303). CONCLUSIONS: Changes in total NEDF consumption were not associated with changes in BMI in children. However, increases in the consumption of sweet bakery products were associated with BMI gain. NEDF are widely recognized as providing poor nutrition yet, their impact in Mexican children BMI seems to be heterogeneous.

Infant Metabolome in Relation to Prenatal DHA Supplementation and Maternal Single-Nucleotide Polymorphism rs174602: Secondary Analysis of a Randomized Controlled Trial in Mexico.

BACKGROUND: Although DHA (22:6n-3) is critical for fetal development, results from randomized controlled trials (RCTs) of prenatal DHA supplementation report inconsistent effects on offspring health. Variants in fatty acid desaturase (FADS) genes that regulate the conversion of n-3 and n-6 essential fatty acids into their biologically active derivatives may explain this heterogeneity. OBJECTIVES: We investigated the effect of prenatal DHA supplementation on the offspring metabolome at age 3 mo and explored differences by maternal FADS single-nucleotide polymorphism (SNP) rs174602. METHODS: Data were obtained from a double-blind RCT in Mexico [POSGRAD (Prenatal Omega-3 Fatty Acid Supplementation and Child Growth and Development)] in which women (18-35 y old) received DHA (400 mg/d) or placebo from mid-gestation until delivery. Using high-resolution MS with LC, untargeted metabolomics was performed on 112 offspring plasma samples. Discriminatory metabolic features were selected via linear regression (P < 0.05) with false discovery rate (FDR) correction (q = 0.2). Interaction by SNP rs174602 was assessed using 2-factor ANOVA. Stratified analyses were performed, where the study population was grouped into carriers (TT, TC; n = 70) and noncarriers (CC; n = 42) of the minor allele. Pathway enrichment analysis was performed with Mummichog (P < 0.05). RESULTS: After FDR correction, there were no differences in metabolic features between infants whose mothers received prenatal DHA (n = 58) and those whose mothers received placebo (n = 54). However, we identified 343 differentially expressed features in the interaction analysis after FDR correction. DHA supplementation positively enriched amino acid and aminosugars metabolism pathways and decreased fatty acid metabolism pathways among offspring of minor allele carriers and decreased metabolites within the tricarboxylic acid cycle and galactose metabolism pathways among offspring of noncarriers. CONCLUSIONS: Our findings demonstrate differences in infant metabolism in response to prenatal DHA supplementation by maternal SNP rs174602 and further support the need to incorporate genetic analysis of FADS polymorphisms into DHA supplementation trials.This trial was registered at clinicaltrials.gov as NCT00646360.

[Pesticide residues in food: health risk and regulation in Veracruz, Mexico]. / Plaguicidas en alimentos: riesgo a la salud y marco regulatorio en Veracruz, México.

Objective. Evaluate compliance with the maximum permissible limits for pesticide residues in food in the state of Veracruz, as well as the risk to human health due to its consumption. Materials and methods. The concentration of pesticide residues in plant products were measured for comparison with the values established as safety limits and the regulatory framework for the use of pesticides. The hazard quotient and its possible effect on health were calculated. Results. 14.8% of the samples exceeded the allowed concentration. We found banned pesticides (methamidophos, monochotophos, triazophos and chlorpyrifos) that exceeded the established references dose, which increase the risk of possible neurological, hepatotoxic and endocrine alterations in health. Conclusions. There is the presence of highly hazardous pesticides, which are prohibited by international environmental conventions due to their impact on health and the environment, which is why their elimination is necessary. The regulatory framework in Mexico must be updated and dynamic as the knowledge of the adverse health effects of pesticides advances.

Maternal obesity leads to long-term altered levels of plasma ceramides in the offspring as revealed by a longitudinal lipidomic study in children.

BACKGROUND/OBJECTIVES: Maternal obesity is associated with increased risk of obesity and other symptoms of the metabolic syndrome in the offspring. Nevertheless, the molecular mechanisms and cellular factors underlying this enhanced disease susceptibility remain to be determined. Here, we aimed at identifying changes in plasma lipids in offspring of obese mothers that might underpin, and serve as early biomarkers of, their enhanced metabolic disease risk. SUBJECTS/METHODS: We performed a longitudinal lipidomic profiling in plasma samples from normal weight, overweight, and obese pregnant women and their children that participated in the Prenatal Omega-3 Fatty Acid Supplementation, Growth, and Development trial conducted in Mexico. At recruitment women were aged between 18 and 35 years and in week 18-22 of pregnancy. Blood samples were collected at term delivery by venipuncture from mothers and from the umbilical cord of their newborns and from the same infants at 4 years old under non-fasting conditions. Lipidomic profiling was done using ultra-performance liquid chromatography high-resolution mass spectrometry. RESULTS: Analysis of the lipidomic data showed that overweight and obese mothers exhibited a significant reduction in the total abundance of ceramides (Cer) in plasma, mainly of Cer (d18:1/20:0), Cer (d18:1/22:0), Cer (d18:1/23:0), and Cer (d18:1/24:0), compared with mothers of normal body weight. This reduction was confirmed by the direct quantification of these and other ceramide species. Similar quantitative differences in the plasma concentration of Cer (d18:1/22:0), Cer (d18:1/23:0), and Cer (d18:1/24:0), were also found between 4-year-old children of overweight and obese mothers compared with children of mothers of normal body weight. Noteworthy, children exhibited equal daily amounts of energy and food intake independently of the BMI of their mothers. CONCLUSIONS: Maternal obesity results in long-lasting changes in plasma ceramides in the offspring suggesting that these lipids might be used as early predictors of metabolic disease risk due to maternal obesity.

Height Trajectory During Early Childhood Is Inversely Associated with Fat Mass in Later Childhood in Mexican Boys.

BACKGROUND: Childhood obesity continues to be a global health problem. Previous research suggests that linear growth retardation or stunting during early childhood increases the risk of obesity, but others have reported that rapid linear growth poses a greater concern than early nutritional status. OBJECTIVE: The objective of this study was to determine if growth trajectories are associated with body composition at age 8-10 y. METHODS: Study participants consisted of 255 girls and 281 boys who participated in a follow-up of the Prenatal Omega-3 Fatty Acid Supplementation and Child Growth and Development (POSGRAD) Study. Sex-specific latent height class (LHC) trajectories were derived from 11 measures of height from birth to 5 y of age and used to calculate 3 distinct growth classes for boys (low, intermediate, and high) and 2 distinct classes for girls (low and high). Body composition at age 8-10 y was estimated using bioelectrical impedance analysis. Multivariable linear regression analysis was used to determine the relationship between growth trajectory classes and fat mass (FM) and fat-free mass (FFM) in late childhood, controlling for confounding factors. RESULTS: In girls, there were no significant associations between LHC and FM or FFM. In boys, relative to the intermediate LHC, the low LHC had higher FM (ß = 0.69 kg; 95% CI: 0.26-1.11 kg) and the high LHC had lower FM (ß = -0.40 kg; 95% CI: -0.76 to -0.05 kg). Boys in the low LHC had significantly less FFM (ß = -0.69 kg; 95% CI: -1.11 to -0.26 kg), and boys in the high LHC had more FFM (ß = 0.40 kg; 95% CI: 0.05-0.76 kg) compared with the intermediate LHC. CONCLUSION: Gain in height among boys, but not girls, in early childhood was associated with lower adiposity in late childhood compared with children with a slower rate of growth. Clinical trial registration number: NCT00646360.

Genetic-Epigenetic Interactions in Asthma Revealed by a Genome-Wide Gene-Centric Search.

OBJECTIVES: There is evidence to suggest that asthma pathogenesis is affected by both genetic and epigenetic variation independently, and there is some evidence to suggest that genetic-epigenetic interactions affect risk of asthma. However, little research has been done to identify such interactions on a genome-wide scale. The aim of this studies was to identify genes with genetic-epigenetic interactions associated with asthma. METHODS: Using asthma case-control data, we applied a novel nonparametric gene-centric approach to test for interactions between multiple SNPs and CpG sites simultaneously in the vicinities of 18,178 genes across the genome. RESULTS: Twelve genes, PF4, ATF3, TPRA1, HOPX, SCARNA18, STC1, OR10K1, UPK1B, LOC101928523, LHX6, CHMP4B, and LANCL1, exhibited statistically significant SNP-CpG interactions (false discovery rate = 0.05). Of these, three have previously been implicated in asthma risk (PF4, ATF3, and TPRA1). Follow-up analysis revealed statistically significant pairwise SNP-CpG interactions for several of these genes, including SCARNA18, LHX6, and LOC101928523 (p = 1.33E-04, 8.21E-04, 1.11E-03, respectively). CONCLUSIONS: Joint effects of genetic and epigenetic variation may play an important role in asthma pathogenesis. Statistical methods that simultaneously account for multiple variations across chromosomal regions may be needed to detect these types of effects on a genome-wide scale.

Relative Weight Gain Through Age 4 Years Is Associated with Increased Adiposity, and Higher Blood Pressure and Insulinemia at 4-5 Years of Age in Mexican Children.

Background: Rapid early weight gain has been associated with increased risk of obesity and cardiometabolic alterations, but evidence in low and middle-income countries is inconclusive. Objective: We evaluated the relation between relative weight gain from 1 to 48 mo with adiposity and cardiometabolic risk factors at 4-5 y of age, and determined if adiposity is a mediator for cardiometabolic alterations. Methods: We studied 428 Mexican children with anthropometric and blood pressure (BP) information from birth to 5 y of age from POSGRAD (Prenatal Omega-3 fatty acid Supplementation and child GRowth And Development), of whom 334 provided measures of adiposity and cardiometabolic risk markers at 4 y. We estimated relative weight gain by means of conditional weight-for-height z scores for the age intervals 1-6, 6-12, 12-24, and 24-48 mo. Associations between relative weight gain and adiposity and cardiometabolic risk markers (lipid profile, triglycerides, insulin, glucose, and BP) were analyzed by multivariate multiple linear models and path analysis. Results: A 1-unit increase in conditional weight-for-height z score within each age interval was positively associated with adiposity at 5 y, with coefficients of 0.43-0.89 for body mass index (BMI) z score, 1.08-3.65 mm for sum of skinfolds, and 1.21-3.87 cm for abdominal circumference (all P < 0.01). Positive associations were documented from ages 6 to 48 mo with systolic BP (coefficient ranges: 1.19-1.78 mm Hg; all P < 0.05) and from ages 12 to 48 mo with diastolic BP (1.28-0.94 mm Hg; P < 0.05) at 5 y. Conditional weight-for-height z scores at 12-24 and 24-48 mo of age were more strongly associated with adiposity and BP relative to younger ages. A unit increase in conditional weight-for-height z scores from 12 to 24 mo was associated with 14% higher insulin levels (P < 0.05) at 4 y. Path analyses documented that the associations of conditional weight gain with BP were mediated by BMI and sum of skinfolds. Conclusion: Relative weight gain at most periods during the first 4 y of life was associated with greater adiposity and higher systolic and diastolic BP at 5 y. These associations with BP were mediated by adiposity. Relative weight gain from 12 to 24 mo was associated with increased serum insulin concentrations at 4 y, but there were no associations with lipid profiles or glucose concentration.

Gene Expression Profiling in Blood Provides Reproducible Molecular Insights into Asthma Control.

RATIONALE: Maintaining optimal symptom control remains the primary objective of asthma treatment. Better understanding of the biologic underpinnings of asthma control may lead to the development of improved clinical and pharmaceutical approaches. OBJECTIVES: To identify molecular pathways and interrelated genes whose differential expression was associated with asthma control. METHODS: We performed gene set enrichment analyses of asthma control in 1,170 adults with asthma, each with gene expression data derived from either whole blood (WB) or unstimulated CD4+ T lymphocytes (CD4), and a self-reported asthma control score representing either the preceding 6 months (chronic) or 7 days (acute). Our study comprised a discovery WB cohort (n = 245, chronic) and three independent, nonoverlapping replication cohorts: a second WB set (n = 448, acute) and two CD4 sets (n = 300, chronic; n = 77, acute). MEASUREMENTS AND MAIN RESULTS: In the WB discovery cohort, we found significant overrepresentation of genes associated with asthma control in 1,106 gene sets from the Molecular Signatures Database (false discovery rate, <5%). Of these, 583 (53%) replicated in at least one replication cohort (false discovery rate, <25%). Suboptimal control was associated with signatures of eosinophilic and granulocytic inflammatory signals, whereas optimal control signatures were enriched for immature lymphocytic patterns. These signatures included two related biologic processes related to activation by TREM-1 (triggering receptor expressed on myeloid cells 1) and lipopolysaccharide. CONCLUSIONS: Together, these results demonstrate the existence of specific, reproducible transcriptomic components in blood that vary with degree of asthma control and implicate a novel biologic target (TREM-1).

Prenatal Docosahexaenoic Acid Supplementation Does Not Affect Nonfasting Serum Lipid and Glucose Concentrations of Offspring at 4 Years of Age in a Follow-Up of a Randomized Controlled Clinical Trial in Mexico.

BACKGROUND: Docosahexaenoic acid (DHA) has regulatory effects on lipid and glucose metabolism. Differences in DHA availability during specific developmental windows may program metabolic changes. OBJECTIVE: We investigated the effects of maternal DHA supplementation during pregnancy on the nonfasting serum lipid and glucose concentrations of offspring at 4 y of age. METHODS: We used data from the Prenatal Omega-3 Fatty Acid Supplementation, Growth, and Development trial, a double-blind randomized controlled trial conducted in Mexico. Pregnant women were supplemented daily with 400 mg DHA or placebo from 18-22 wk of gestation to delivery. The primary outcomes of the trial were offspring growth and neurological development. Nonfasting blood samples were obtained from the offspring at 4 y of age. We analyzed serum total, HDL, non-HDL, and LDL cholesterol; the total-to-HDL cholesterol ratio; apolipoprotein B (apoB); triglycerides; glucose; and insulin as secondary outcomes and compared their concentrations between treatment groups. RESULTS: Data from 524 offspring were available. The women were compliant with the intervention based on pill counts and changes in cord blood and breast milk DHA concentrations. None of the between-group differences (DHA compared with placebo), adjusted for maternal height and time since last food intake, were significant (P range 0.27-0.83). Means (95% CIs) were as follows: total cholesterol (TC), 1.73 mg/dL (-2.63, 6.09 mg/dL); HDL cholesterol, 0.66 mg/dL (-1.07, 2.39 mg/dL); non-HDL cholesterol, 1.77 mg/dL (-1.83, 5.37 mg/dL); LDL cholesterol, 1.62 mg/dL (-2.21, 5.45 mg/dL); TC:HDL ratio, 0.01 (-0.09, 0.11); apoB, -0.15 mg/dL (-2.78, 2.48 mg/dL); triglycerides, 0.21 mg/dL (-10.93, 10.52 mg/dL); glucose, -0.67 mg/dL (-2.46, 1.11 mg/dL); and insulin, 0.62 µU/mL (-0.88, 2.11 µU/mL). CONCLUSION: Prenatal DHA supplementation does not affect nonfasting serum lipid and glucose concentrations of offspring at 4 y of age. This trial was registered at clinicaltrials.gov as NCT00646360.

[Oxidative stress, lung function and exposure to air pollutants in Mexican schoolchildren with and without asthma]. / Estrés oxidativo, función pulmonar y exposición a contaminantes atmosféricos en escolares mexicanos con y sin asma.

OBJECTIVE.: To assess the association between the air pollutants exposure on markers of oxidative stress and lung function in schoolchildren with and without asthma from Salamanca and Leon Guanajuato, Mexico. MATERIALS AND METHODS: We realized determinations of oxidative stress biomarkers and lung function tests in 314 schoolchildren. Information of air pollutants (O3, SO2, CO, PM2.5 and PM10) were obtained from monitoring stations and multiple linear regression models were run to assess the association. RESULTS: An increase of 0.09 pmol in conjugated dienes was observed by exposure to PM10 lag 1 in asthmatics from Salamanca (p<0.05). The exposure to O3 during the same day increased the concentration of Lipohydroperoxides in 4.38 nmol in asthmatics of Salamanca, as well as in 2.31 nmol by exposure to PM10 lag 2 (p<0.05). The forced vital capacity decreased by 138 and 203 ml in children without asthma, respectively, due to exposure to carbon monoxide (p<0.05). CONCLUSIONS: Exposure to air pollutants increase oxidative stress and decreased lung function in schoolchildren, with and without asthma.

OBJETIVO: Evaluar la asociación entre la exposición a contaminantes atmosféricos y marcadores de estrés oxidativo, por un lado, y la función pulmonar, por el otro, en escolares, con y sin asma, de las ciudades de Salamanca y León, en Guanajuato, México. MATERIAL Y MÉTODOS: Se realizaron determinaciones de marcadores de estrés oxidativo y pruebas de función pulmonar en 314 escolares, y se obtuvo información sobre contaminantes atmosféricos (ozono, dióxido de azufre, monóxido de carbono y partículas menores de 2.5 µm y menores de 10 µm) de las estaciones de monitoreo correspondientes. Para evaluar la asociación se corrieron modelos de regresión lineal múltiple. RESULTADOS: Con un día de retraso a la exposición a partículas menores de 10 µm (PM10), se observó un incremento de 0.09 pmol en los dienos conjugados entre niños asmáticos de Salamanca (p<0.05). La exposición a ozono durante el mismo día incrementó la concentración de lipo-hidroperóxidos en 4.38 nmol entre asmáticos de Salamanca, así como en 2.31 nmol por la exposición a PM10 para dos días de retraso (p<0.05). La capacidad vital forzada disminuyó 138 y 203 ml en niños sin asma, respectivamente, por la exposición a monóxido de carbono (p<0.05). CONCLUSIONES: La exposición a contaminantes atmosféricos incrementa el estrés oxidativo y disminuye la función pulmonar en escolares con y sin asma.

Glucocorticoid genes and the developmental origins of asthma susceptibility and treatment response.

Antenatal corticosteroids enhance lung maturation. However, the importance of glucocorticoid genes on early lung development, asthma susceptibility, and treatment response remains unknown. We investigated whether glucocorticoid genes are important during lung development and their role in asthma susceptibility and treatment response. We identified genes that were differentially expressed by corticosteroids in two of three genomic datasets: lymphoblastoid cell lines of participants in the Childhood Asthma Management Program, a glucocorticoid chromatin immunoprecipitation/RNA sequencing experiment, or a murine model; these genes made up the glucocorticoid gene set (GCGS). Using gene expression profiles from 38 human fetal lungs and C57BL/6J murine fetal lungs, we identified developmental genes that were in the top 5% of genes contributing to the top three principal components (PCs) most highly associated with post-conceptional age. Glucocorticoid genes that were enriched in this set of developmental genes were then included in the developmental glucocorticoid gene set (DGGS). We then investigated whether glucocorticoid genes are important during lung development, and their role in asthma susceptibility and treatment response. A total of 232 genes were included in the GCGS. Analysis of gene expression demonstrated that glucocorticoid genes were enriched in lung development (P = 7.02 × 10(-26)). The developmental GCGS was enriched for genes that were differentially expressed between subjects with asthma and control subjects (P = 4.26 × 10(-3)) and were enriched after treatment of subjects with asthma with inhaled corticosteroids (P < 2.72 × 10(-4)). Our results show that glucocorticoid genes are overrepresented among genes implicated in fetal lung development. These genes influence asthma susceptibility and treatment response, suggesting their involvement in the early ontogeny of asthma.

Breastfeeding status at age 3 months is associated with adiposity and cardiometabolic markers at age 4 years in Mexican children.

BACKGROUND: The effect of breastfeeding (BF) on cardiometabolic risk factors is not well characterized. OBJECTIVE: The objective was to assess the association of BF status at 3 mo and duration with adiposity and cardiometabolic markers at 4 y. METHODS: We studied 727 children with prospectively collected BF information and anthropometric measurements at 4 y, of whom 524 provided a nonfasting blood sample. BF status at 3 mo was classified as exclusive or predominant (EBF-PreBF), partial (PaBF), or nonbreastfeeding (NBF). Total duration of any BF was classified as <3 mo, 3- 6 mo, >6 to 12 mo, and >12 mo. We modeled associations of BF with body mass index (BMI; in kg/m(2)), serum total cholesterol and low-density lipoprotein (LDL) cholesterol, triglycerides (TGs), and insulin at 4 y. RESULTS: Children who were NBF or PaBF at 3 mo had higher BMI [0.46 (95% CI: 0.16, 0.76) and 0.31 (95% CI: 0.07, 0.54), respectively] than the EBF-PreBF group (P < 0.01). NBF children had higher total cholesterol (8.02 mg/dL; 95% CI: 1.39, 14.64; P = 0.02) than children who were EBF-PreBF. LDL cholesterol (5.04 mg/dL; 95% CI: -0.72, 10.81) and TGs (12% change; 95% CI: -0.01, 0.24) showed similar patterns. An inverse association between EBF-PreBF and insulin, mediated through abdominal circumference, was documented (P < 0.05). Children breastfed <3 mo had higher BMI (0.44; 95% CI: 0.11, 0.77) at 4 y than children breastfed for >12 mo. CONCLUSION: EBF and PreBF at 3 mo were associated with lower adiposity and serum total cholesterol in children at 4 y. In addition, BF >12 mo was associated with lower adiposity. These data confirm the importance of exclusive BF and prolonged BF for later cardiometabolic health.

Prenatal Supplementation with Docosahexaenoic Acid Has No Effect on Growth through 60 Months of Age.

BACKGROUND: Prenatal supplementation with docosahexaenoic acid (DHA) has been shown to increase birth size, but it is unclear whether these differences translate into improved postnatal growth. OBJECTIVE: We assessed the effect of prenatal supplementation with DHA on offspring weight, length, and body mass index (BMI) through 60 mo of age. METHODS: We examined growth patterns (height, weight, and BMI) in a cohort of 802 Mexican children whose mothers participated in a randomized, controlled trial of daily supplementation with 400 mg/d of DHA or a placebo from week 18-22 of gestation through delivery, with the use of a longitudinal multilevel model of growth. RESULTS: Overall, means ± SDs of height-, weight-, and BMI-for-age z scores relative to WHO growth standards at 60 mo were -0.49 ± 0.91, -1.15 ± 1.07 and 0.13 ± 1.11, respectively. There were no significant differences by treatment group (all P > 0.05) for height, weight, or BMI at any age through 60 mo. Similarly, DHA did not affect the average growth or the trajectories for these measures through 60 mo. CONCLUSION: Prenatal DHA supplementation did not affect height, weight, or BMI through 60 mo of age. This trial was registered at clinicaltrials.gov as NCT00646360.

Indoor determinants of dustborne allergens in Mexican homes.

Exposure to indoor allergens represents a significant risk factor for allergies and asthma in several parts of the world. In Mexico, few studies have evaluated indoor allergens, including cat, dog, and mouse allergens and the factors that predict their presence. This study evaluates the main environmental and household predictors of high prenatal allergen levels and multiple allergen exposures in a birth cohort from Mexico City. A cross-sectional study was conducted as part of a birth cohort study of 1094 infants recruited during pregnancy and followed until delivery. We collected dust samples in a subset of 264 homes and assessed environmental factors. Der p 1, Der f 1, dust mite group 2, Fel d 1, Can f 1, Rat n 1, Mus m 1, and Bla g 2 concentrations in dust samples were measured using immunoassays. To define detectable allergen levels, the lowest limits of detection for each allergen were taken as cutoff points. Overall allergen exposure was considered high when four or more allergens exceeded detectable levels in the same household. Logistic regression was used for predictive models. Eighty-five percent of homes had at least one allergen in dust over the detection limit, 52.1% had high exposure (four or more allergens above detectable limits), and 11.7% of homes had detectable levels for more than eight allergens. Der p 1, Der p 2, Mus m 1, and Fel d 1 were the most frequent allergens detected. Each allergen had both common and distinct predictors. The main predictors of a high multiple allergen index were the size of the home, pesticide use, mother's age, mother as homemaker, and season. Increased indoor environmental allergen exposure is mainly related to sociodemographic factors and household cleaning.

Dietary supplementation with polyunsaturated fatty acid during pregnancy modulates DNA methylation at IGF2/H19 imprinted genes and growth of infants.

Epigenetic regulation of imprinted genes is regarded as a highly plausible explanation for linking dietary exposures in early life with the onset of diseases during childhood and adulthood. We sought to test whether prenatal dietary supplementation with docosahexaenoic acid (DHA) during pregnancy may modulate epigenetic states at birth. This study was based on a randomized intervention trial conducted in Mexican pregnant women supplemented daily with 400 mg of DHA or a placebo from gestation week 18-22 to parturition. We applied quantitative profiling of DNA methylation states at IGF2 promoter 3 (IGF2 P3), IGF2 differentially methylated region (DMR), and H19 DMR in cord blood mononuclear cells of the DHA-supplemented group (n = 131) and the control group (n = 130). In stratified analyses, DNA methylation levels in IGF2 P3 were significantly higher in the DHA group than the control group in preterm infants (P = 0.04). We also observed a positive association between DNA methylation levels and maternal body mass index; IGF2 DMR methylation was higher in the DHA group than the control group in infants of overweight mothers (P = 0.03). In addition, at H19 DMR, methylation levels were significantly lower in the DHA group than the control group in infants of normal weight mothers (P = 0.01). Finally, methylation levels at IGF2/H19 imprinted regions were associated with maternal BMI. These findings suggest that epigenetic mechanisms may be modulated by DHA, with potential impacts on child growth and development.

Effect of socioeconomic status on the association between air pollution and mortality in Bogota, Colombia.

OBJECTIVE: To evaluate the modification effect of socioeconomic status (SES) on the association between acute exposure to particulate matter less than 10 microns in aerodynamic diameter (PM10) and mortality in Bogota, Colombia. MATERIALS AND METHODS: A time-series ecological study was conducted (1998-2006). The localities of the cities were stratified using principal components analysis, creating three levels of aggregation that allowed for the evaluation of the impact of SES on the relationship between mortality and air pollution. RESULTS: For all ages, the change in the mortality risk for all causes was 0.76% (95%CI 0.27-1.26) for SES I (low), 0.58% (95%CI 0.16-1.00) for SES II (mid) and -0.29% (95%CI -1.16-0.57) for SES III (high) per 10µg/m³ increment in the daily average of PM10 on day of death. CONCLUSIONS: The results suggest that SES significantly modifies the effect of environmental exposure to PM10 on mortality from all causes and respiratory causes.

Effect of particulate matter less than 10µm (PM10) on mortality in Bogota, Colombia: a time-series analysis, 1998-2006.

OBJECTIVE: To analyze the association between daily mortality from different causes and acute exposure to particulate matter less than 10 microns in aerodynamic diameter (PM10), in Bogota, Colombia. MATERIALS AND METHODS: A time-series ecological study was conducted from 1998 to 2006. The association between mortality (due to different causes) and exposure was analyzed using single and distributed lag models and adjusting for potential confounders. RESULTS: For all ages, the cumulative effect of acute mortality from all causes and respiratory causes increased 0.71% (95%CI 0.46-0.96) and 1.43% (95%CI 0.85-2.00), respectively, per 10µg/m³ increment in daily average PM10 with a lag of three days before death. Cumulative effect of mortality from cardiovascular causes was -0.03% (95%CI -0.49-0.44%) with the same lag. CONCLUSIONS: The results suggest an association between an increase in PM10 concentrations and acute mortality from all causes and respiratory causes.

Prenatal Arsenic Exposure on DNA Methylation of C18ORF8 and ADAMTS9 Genes of Newborns from the POSGRAD Birth Cohort Study.

Exposure to arsenic (As) is a public health problem associated with cancer (skin and colon) and it has been reported that epigenetic changes may be a potential mechanism of As carcinogenesis. It is pertinent to evaluate this process in genes that have been associated with cancer, such as ADAMTS9 and C18ORF8. Gestation and delivery data were obtained from the POSGRAD study. Exposure to As was measured in urine during pregnancy. Gene methylation was performed by sodium bisulfite sequencing; 26 CpG sites for the C18ORF8 gene and 21 for ADAMTS9 were analyzed. These sites are located on the CpG islands near the start of transcription. Sociodemographic characteristics were obtained by a questionnaire. The statistical analysis was performed using multiple linear regression models adjusted for potential confounders. Newborns with an As exposure above 49.4 µg g-1 showed a decrease of 0.21% on the methylation rate in the sites CpG15, CpG19, and CpG21 of the C18ORF8 gene (adjusted ß = -0.21, p-value = 0.02). No statistically significant association was found between prenatal exposure to As and methylation of the ADAMTS9 gene. Prenatal exposure to As was associated with decreased DNA methylation at the CpG15, CpG19, and CpG21 sites of the C18ORF8 gene. These sites can provide information to elucidate epigenetic mechanisms associated with prenatal exposure to As and cancer.

Ozone exposure, vitamin C intake, and genetic susceptibility of asthmatic children in Mexico City: a cohort study.

BACKGROUND: We previously reported that asthmatic children with GSTM1 null genotype may be more susceptible to the acute effect of ozone on the small airways and might benefit from antioxidant supplementation. This study aims to assess the acute effect of ozone on lung function (FEF(25-75)) in asthmatic children according to dietary intake of vitamin C and the number of putative risk alleles in three antioxidant genes: GSTM1, GSTP1 (rs1695), and NQO1 (rs1800566). METHODS: 257 asthmatic children from two cohort studies conducted in Mexico City were included. Stratified linear mixed models with random intercepts and random slopes on ozone were used. Potential confounding by ethnicity was assessed. Analyses were conducted under single gene and genotype score approaches. RESULTS: The change in FEF(25-75) per interquartile range (60 ppb) of ozone in persistent asthmatic children with low vitamin C intake and GSTM1 null was -91.2 ml/s (p = 0.06). Persistent asthmatic children with 4 to 6 risk alleles and low vitamin C intake showed an average decrement in FEF(25-75) of 97.2 ml/s per 60 ppb of ozone (p = 0.03). In contrast in children with 1 to 3 risk alleles, acute effects of ozone on FEF25-75 did not differ by vitamin C intake. CONCLUSIONS: Our results provide further evidence that asthmatic children predicted to have compromised antioxidant defense by virtue of genetic susceptibility combined with deficient antioxidant intake may be at increased risk of adverse effects of ozone on pulmonary function.