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Duncan Thomas

Publications and source records attributed to Duncan Thomas.

At least 19 recordsLinked to original sources
PubMed2006

Bayesian modeling of air pollution health effects with missing exposure data.

The authors propose a new statistical procedure that utilizes measurement error models to estimate missing exposure data in health effects assessment. The method detailed in this paper follows a Bayesian framework that allows estimation of various parameters of the model in the presence of missing covariates in an informative way. The authors apply this methodology to study the effect of household-level long-term air pollution exposures on lung function for subjects from the Southern California Children's Health Study pilot project, conducted in the year 2000. Specifically, they propose techniques to examine the long-term effects of nitrogen dioxide (NO2) exposure on children's lung function for persons living in 11 southern California communities. The effect of nitrogen dioxide exposure on various measures of lung function was examined, but, similar to many air pollution studies, no completely accurate measure of household-level long-term nitrogen dioxide exposure was available. Rather, community-level nitrogen dioxide was measured continuously over many years, but household-level nitrogen dioxide exposure was measured only during two 2-week periods, one period in the summer and one period in the winter. From these incomplete measures, long-term nitrogen dioxide exposure and its effect on health must be inferred. Results show that the method improves estimates when compared with standard frequentist approaches.

Air Pollutants↗
PubMed2006

Testing metabolic ecology theory for allometric scaling of tree size, growth and mortality in tropical forests.

The theory of metabolic ecology predicts specific relationships among tree stem diameter, biomass, height, growth and mortality. As demographic rates are important to estimates of carbon fluxes in forests, this theory might offer important insights into the global carbon budget, and deserves careful assessment. We assembled data from 10 old-growth tropical forests encompassing censuses of 367 ha and > 1.7 million trees to test the theory's predictions. We also developed a set of alternative predictions that retained some assumptions of metabolic ecology while also considering how availability of a key limiting resource, light, changes with tree size. Our results show that there are no universal scaling relationships of growth or mortality with size among trees in tropical forests. Observed patterns were consistent with our alternative model in the one site where we had the data necessary to evaluate it, and were inconsistent with the predictions of metabolic ecology in all forests.

Biometry↗
PubMed2006

Comparing tropical forest tree size distributions with the predictions of metabolic ecology and equilibrium models.

Tropical forests vary substantially in the densities of trees of different sizes and thus in above-ground biomass and carbon stores. However, these tree size distributions show fundamental similarities suggestive of underlying general principles. The theory of metabolic ecology predicts that tree abundances will scale as the -2 power of diameter. Demographic equilibrium theory explains tree abundances in terms of the scaling of growth and mortality. We use demographic equilibrium theory to derive analytic predictions for tree size distributions corresponding to different growth and mortality functions. We test both sets of predictions using data from 14 large-scale tropical forest plots encompassing censuses of 473 ha and > 2 million trees. The data are uniformly inconsistent with the predictions of metabolic ecology. In most forests, size distributions are much closer to the predictions of demographic equilibrium, and thus, intersite variation in size distributions is explained partly by intersite variation in growth and mortality.

Biomass↗
PubMed2006

Dog ownership enhances symptomatic responses to air pollution in children with asthma.

BACKGROUND: Experimental data suggest that asthma exacerbation by ambient air pollutants is enhanced by exposure to endotoxin and allergens; however, there is little supporting epidemiologic evidence. METHODS: We evaluated whether the association of exposure to air pollution with annual prevalence of chronic cough, phlegm production, or bronchitis was modified by dog and cat ownership (indicators of allergen and endotoxin exposure). The study population consisted of 475 Southern California children with asthma from a longitudinal cohort of participants in the Children's Health Study. We estimated average annual ambient exposure to nitrogen dioxide, ozone, particulate matter < 10, 2.5, and 10-2.5 microm in aerodynamic diameter (PM10, PM2.5, and PM10-2.5, respectively), elemental and organic carbon, and acid vapor from monitoring stations in each of the 12 study communities. Multivariate models were used to examine the effect of yearly variation of each pollutant. Effects were scaled to the variability that is common for each pollutant in representative communities in Southern California. RESULTS: Among children owning a dog, there were strong associations between bronchitic symptoms and all pollutants examined. Odds ratios ranged from 1.30 per 4.2 microg/m3 for PM10-2.5 [95% confidence interval (CI), 0.91-1.87) to 1.91 per 1.2 microg/m3 for organic carbon (95% CI, 1.34-2.71). Effects were somewhat larger among children who owned both a cat and dog. There were no effects or small effects with wide CIs among children without a dog and among children who owned only a cat. CONCLUSION: Our results suggest that dog ownership, a source of residential exposure to endotoxin, may worsen the relationship between air pollution and respiratory symptoms in asthmatic children.

Adolescent↗
PubMed2006

Traffic, susceptibility, and childhood asthma.

Results from studies of traffic and childhood asthma have been inconsistent, but there has been little systematic evaluation of susceptible subgroups. In this study, we examined the relationship of local traffic-related exposure and asthma and wheeze in southern California school children (5-7 years of age). Lifetime history of doctor-diagnosed asthma and prevalent asthma and wheeze were evaluated by questionnaire. Parental history of asthma and child's history of allergic symptoms, sex, and early-life exposure (residence at the same home since 2 years of age) were examined as susceptibility factors. Residential exposure was assessed by proximity to a major road and by modeling exposure to local traffic-related pollutants. Residence within 75 m of a major road was associated with an increased risk of lifetime asthma [odds ratio (OR)=1.29; 95% confidence interval (CI), 1.01-1.86], prevalent asthma (OR=1.50; 95% CI, 1.16-1.95), and wheeze (OR=1.40; 95% CI, 1.09-1.78). Susceptibility increased in long-term residents with no parental history of asthma for lifetime asthma (OR=1.85; 95% CI, 1.11-3.09), prevalent asthma (OR=2.46; 95% CI, 0.48-4.09), and recent wheeze (OR=2.74; 95% CI, 1.71-4.39). The higher risk of asthma near a major road decreased to background rates at 150-200 m from the road. In children with a parental history of asthma and in children moving to the residence after 2 years of age, there was no increased risk associated with exposure. Effect of residential proximity to roadways was also larger in girls. A similar pattern of effects was observed with traffic-modeled exposure. These results indicate that residence near a major road is associated with asthma. The reason for larger effects in those with no parental history of asthma merits further investigation.

Air Pollutants↗
PubMed2005

Can expanding access to basic healthcare improve children's health status? Lessons from Indonesia's 'midwife in the village' programme.

In the 1990s, the Indonesian government placed over 50,000 midwives in communities throughout the country. We examine how this expansion in health services affected children's height-for-age. To address the problem that midwives were not randomly allocated to communities, the estimation exploits the biology of childhood growth, the timing of the introduction of midwives to communities, and rich longitudinal data. The evidence indicates that the nutritional status of children fully exposed to a midwife during early childhood is significantly better than that of their peers of the same age and cohort in communities without a midwife. The former are also better off than children assessed at the same age from the same communities but who were born before the midwife arrived. Within communities, the improvement in nutritional status across cohorts is greater where midwives were introduced than where they were not. This result is robust to the inclusion of community fixed effects.

Body Height↗
PubMed2005

Ambient air pollution and atherosclerosis in Los Angeles.

Associations have been found between long-term exposure to ambient air pollution and cardiovascular morbidity and mortality. The contribution of air pollution to atherosclerosis that underlies many cardiovascular diseases has not been investigated. Animal data suggest that ambient particulate matter (PM) may contribute to atherogenesis. We used data on 798 participants from two clinical trials to investigate the association between atherosclerosis and long-term exposure to ambient PM up to 2.5 microm in aerodynamic diameter (PM2.5). Baseline data included assessment of the carotid intima-media thickness (CIMT), a measure of subclinical atherosclerosis. We geocoded subjects' residential areas to assign annual mean concentrations of ambient PM2.5. Exposure values were assigned from a PM2.5 surface derived from a geostatistical model. Individually assigned annual mean PM2.5 concentrations ranged from 5.2 to 26.9 microg/m3 (mean, 20.3). For a cross-sectional exposure contrast of 10 microg/m3 PM2.5, CIMT increased by 5.9% (95% confidence interval, 1-11%). Adjustment for age reduced the coefficients, but further adjustment for covariates indicated robust estimates in the range of 3.9-4.3% (p-values, 0.05-0.1). Among older subjects (greater than or equal to 60 years of age), women, never smokers, and those reporting lipid-lowering treatment at baseline, the associations of PM2.5 and CIMT were larger with the strongest associations in women 60 years of age (15.7%, 5.7-26.6%). These results represent the first epidemiologic evidence of an association between atherosclerosis and ambient air pollution. Given the leading role of cardiovascular disease as a cause of death and the large populations exposed to ambient PM2.5, these findings may be important and need further confirmation.

Adult↗
PubMed2005

Health consequences of forest fires in Indonesia.

We combined data from a population-based longitudinal survey with satellite measures of aerosol levels to assess the impact of smoke from forest fires that blanketed the Indonesian islands of Kalimantan and Sumatra in late 1997 on adult health. To account for unobserved differences between haze and nonhaze areas, we compared changes in the health of individual respondents. Between 1993 and 1997, individuals who were exposed to haze experienced greater increases in difficulty with activities of daily living than did their counterparts in nonhaze areas. The results for respiratory and general health, although more complicated to interpret, suggest that haze had a negative impact on these dimensions of health.

Activities of Daily Living↗
PubMed2004

The effect of air pollution on lung development from 10 to 18 years of age.

BACKGROUND: Whether exposure to air pollution adversely affects the growth of lung function during the period of rapid lung development that occurs between the ages of 10 and 18 years is unknown. METHODS: In this prospective study, we recruited 1759 children (average age, 10 years) from schools in 12 southern California communities and measured lung function annually for eight years. The rate of attrition was approximately 10 percent per year. The communities represented a wide range of ambient exposures to ozone, acid vapor, nitrogen dioxide, and particulate matter. Linear regression was used to examine the relationship of air pollution to the forced expiratory volume in one second (FEV(1)) and other spirometric measures. RESULTS: Over the eight-year period, deficits in the growth of FEV(1) were associated with exposure to nitrogen dioxide (P=0.005), acid vapor (P=0.004), particulate matter with an aerodynamic diameter of less than 2.5 microm (PM(2.5)) (P=0.04), and elemental carbon (P=0.007), even after adjustment for several potential confounders and effect modifiers. Associations were also observed for other spirometric measures. Exposure to pollutants was associated with clinically and statistically significant deficits in the FEV(1) attained at the age of 18 years. For example, the estimated proportion of 18-year-old subjects with a low FEV(1) (defined as a ratio of observed to expected FEV(1) of less than 80 percent) was 4.9 times as great at the highest level of exposure to PM(2.5) as at the lowest level of exposure (7.9 percent vs. 1.6 percent, P=0.002). CONCLUSIONS: The results of this study indicate that current levels of air pollution have chronic, adverse effects on lung development in children from the age of 10 to 18 years, leading to clinically significant deficits in attained FEV(1) as children reach adulthood.

Adolescent↗
PubMed2004

Two-Stage sampling designs for gene association studies.

We consider two-stage case-control designs for testing associations between single nucleotide polymorphisms (SNPs) and disease, in which a subsample of subjects is used to select a panel of "tagging" SNPs that will be considered in the main study. We propose a pseudolikelihood [Pepe and Flemming, 1991: JASA 86:108-113] that combines the information from both the main study and the substudy to test the association with any polymorphism in the original set. SNP-tagging [Chapman et al., 2003: Hum Hered 56:18-31] and haplotype-tagging [Stram et al., 2003a; Hum Hered 55:27-36] approaches are compared. We show that the cost-efficiency of such a design for estimating the relative risk associated with the causal polymorphism can be considerably better than for a single-stage design, even if the causal polymorphism is not included in the tag-SNP set. We also consider the optimal selection of cases and controls in such designs and the relative efficiency for estimating the location of a causal variant in linkage disequilibrium mapping. Nevertheless, as the cost of high-volume genotyping plummets and haplotype tagging information from the International HapMap project [Gibbs et al., 2003; Nature 426:789-796] rapidly accumulates in public databases, such two-stage designs may soon become unnecessary.

Case-Control Studies↗
PubMed2004

A survey of current Bayesian gene mapping methods.

Recently, there has been much interest in the use of Bayesian statistical methods for performing genetic analyses. Many of the computational difficulties previously associated with Bayesian analysis, such as multidimensional integration, can now be easily overcome using modern high-speed computers and Markov chain Monte Carlo (MCMC) methods. Much of this new technology has been used to perform gene mapping, especially through the use of multi-locus linkage disequilibrium techniques. This review attempts to summarise some of the currently available methods and the software available to implement these methods.

Bayes Theorem↗
PubMed2003

Multiple imputation methods for longitudinal blood pressure measurements from the Framingham Heart Study.

Missing data are a great concern in longitudinal studies, because few subjects will have complete data and missingness could be an indicator of an adverse outcome. Analyses that exclude potentially informative observations due to missing data can be inefficient or biased. To assess the extent of these problems in the context of genetic analyses, we compared case-wise deletion to two multiple imputation methods available in the popular SAS package, the propensity score and regression methods. For both the real and simulated data sets, the propensity score and regression methods produced results similar to case-wise deletion. However, for the simulated data, the estimates of heritability for case-wise deletion and the two multiple imputation methods were much lower than for the complete data. This suggests that if missingness patterns are correlated within families, then imputation methods that do not allow this correlation can yield biased results.

Adult↗
PubMed2003

Fine-scale mapping of disease genes with multiple mutations via spatial clustering techniques.

We present a method to perform fine mapping by placing haplotypes into clusters on the basis of risk. Each cluster has a haplotype "center." Cluster allocation is defined according to haplotype centers, with each haplotype assigned to the cluster with the "closest" center. The closeness of two haplotypes is determined by a similarity metric that measures the length of the shared segment around the location of a putative functional mutation for the particular cluster. Our method allows for missing marker information but still estimates the risks of complete haplotypes without resorting to a one-marker-at-a-time analysis. The dimensionality issues that can occur in haplotype analyses are removed by sampling over the haplotype space, allowing for estimation of haplotype risks without explicitly assigning a parameter to each haplotype to be estimated. In this way, we are able to handle haplotypes of arbitrary size. Furthermore, our clustering approach has the potential to allow us to detect the presence of multiple functional mutations.

Algorithms↗
PubMed2003

Prospective study of air pollution and bronchitic symptoms in children with asthma.

The relationship of bronchitic symptoms to ambient particulate matter and to particulate elemental and organic carbon (OC), nitrogen dioxide (NO2), and other gaseous pollutants was examined in a cohort of children with asthma in 12 Southern California communities. Symptoms, assessed yearly by questionnaire from 1996 to 1999, were associated with the yearly variability of particulate matter with aerodynamic diameter less than 2.5 microg (odds ratio [OR] 1.09/microg/m3; 95% confidence interval [CI] 1.01-1.17), OC (OR 1.41/microg/m3; 95% CI 1.12-1.78), NO2 (OR 1.07/ppb; 95% CI 1.02-1.13), and ozone (OR 1.06/ppb; 95% CI 1.00-1.12). The ORs associated with yearly within-community variability in air pollution were larger than the effect of the between-community 4-year average concentrations. In two pollutant models, the effects of yearly variation in OC and NO2 were only modestly reduced by adjusting for other pollutants, except in a model containing both OC and NO2; the effects of all other pollutants were reduced after adjusting for OC or NO2. We conclude that OC and NO2 deserve greater attention as potential causes of the chronic symptoms of bronchitis in children with asthma and that previous cross-sectional studies may have underestimated the risks associated with air pollution.

Adolescent↗
PubMed2003

Application of Bayesian spatial statistical methods to analysis of haplotypes effects and gene mapping.

We propose a method to analyze haplotype effects using ideas derived from Bayesian spatial statistics. We assume that two haplotypes that are similar to one another in structure are likely to have similar risks, and define a distance metric to specify the appropriate level of closeness between the two haplotypes. Through the choice of distance metric, varying levels of population genetics theory can be incorporated into the modeling process, including some that allow estimation of the location of the disease causing mutation(s). This location can be estimated, along with the other parameters of the model, using Markov chain Monte Carlo (MCMC) estimation methods. We demonstrate the effectiveness of the model on two real datasets, a well-known dataset used to fine-map the gene for cystic fibrosis, and one used to localize the gene for Friedreich's ataxia.

Bayes Theorem↗
PubMed2002

Reporting, appraising, and integrating data on genotype prevalence and gene-disease associations.

The recent completion of the first draft of the human genome sequence and advances in technologies for genomic analysis are generating tremendous opportunities for epidemiologic studies to evaluate the role of genetic variants in human disease. Many methodological issues apply to the investigation of variation in the frequency of allelic variants of human genes, of the possibility that these influence disease risk, and of assessment of the magnitude of the associated risk. Based on a Human Genome Epidemiology workshop, a checklist for reporting and appraising studies of genotype prevalence and studies of gene-disease associations was developed. This focuses on selection of study subjects, analytic validity of genotyping, population stratification, and statistical issues. Use of the checklist should facilitate the integration of evidence from these studies. The relation between the checklist and grading schemes that have been proposed for the evaluation of observational studies is discussed. Although the limitations of grading schemes are recognized, a robust approach is proposed. Other issues in the synthesis of evidence that are particularly relevant to studies of genotype prevalence and gene-disease association are discussed, notably identification of studies, publication bias, criteria for causal inference, and the appropriateness of quantitative synthesis.

Case-Control Studies↗
PubMed2002

Association between air pollution and lung function growth in southern California children: results from a second cohort.

A cohort of 1,678 Southern California children, enrolled as fourth graders in 1996, was followed for 4 years to determine whether the growth in lung function of the children was associated with their exposure to ambient air pollutants. These subjects comprised the second cohort of fourth grade children participating in the Children's Health Study. Significant deficits in lung function growth rate were associated with exposure to acid vapor, NO(2), particles with aerodynamic diameter less than 2.5 microm (PM(2.5)), and elemental carbon. For example, the average annual growth rates of maximal midexpiratory flow and forced expiratory volume in 1 second were reduced by approximately 11% (p = 0.005) and 5% (p = 0.03), respectively, across the observed range of acid exposure. Exposure to acid vapor was also associated with reductions in the ratio of maximal midexpiratory flow to forced vital capacity (p = 0.02), whereas exposure to ozone was correlated with reduced growth in peak flow rate (p = 0.006). Larger deficits in lung function growth rate were observed in children who reported spending more time outdoors. These findings provide important replication of our previous findings of an effect of air pollution on lung function growth that were based on the first fourth-grade cohort from the Children's Health Study (Am J Respir Crit Care Med 2000;162:1383-1390).

Air Pollutants↗