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National surveys of the exposure of non-smokers to secondhand smoke based on serum cotinine analyses have consistently identified certain groups within the population including children, males and non-Hispanic Blacks as having relatively greater exposure. Although these differences in mean serum cotinine concentrations probably represent differences in exposure of individuals in their daily lives, it is also possible that metabolic or other differences in response might influence the results. To better define the nature of those findings, we have examined the response of 40 non-smokers including both men and women and African-Americans and whites to sidestream (SS) cigarette smoke generated by a smoking machine under controlled conditions. In this study, participants were exposed to aged, diluted SS smoke (ADSS) generated in an environmental chamber with a mean air nicotine concentration of 140 μg m-3 and 8.6 ppm CO for 4 h. Salivary cotinine was measured every 30 min, and serum cotinine samples were taken prior to, and 2 h after exposure. Urinary nicotine metabolites and NNAL, a tobacco-specific nitrosamine, and 4-aminobiphenyl (4-AB) haemoglobin adducts were also measured prior to and 2 h following the exposure. Under these uniform, controlled conditions, we found a similar response to ADSS smoke exposure among all the participants. In all cases a significant increase in biomarker concentration was noted following exposure, and the short-term increases in salivary cotinine concentration were quite similar at approximately 12 pg ml-1 min-1 among the groups. In this small study, no significant differences by gender or race were seen in the mean increases observed in cotinine, NNAL or 4-AB adducts following 4 h of exposure. Thus, our results are most consistent with a relatively uniform response in tobacco biomarker concentrations following short-term exposure to ADSS tobacco smoke, and suggest that biomarker measurements are capable of effectively indicating increases in exposure among groups of non-smokers. [ABSTRACT FROM AUTHOR]

OBJECTIVE: In a study to identify exposures associated with 15 cases of childhood leukemia, we found levels of tungsten, arsenic, and dichlorodiphenyldichloroethylene in participants to be higher than mean values reported in the National Report on Human Exposure to Environmental Chemicals. Because case and comparison families had similar levels of these contaminants, we conducted genetic studies to identify gene polymorphisms that might have made case children more susceptible than comparison children to effects of the exposures. DESIGN: We compared case with comparison children to determine whether differences existed in the frequency of polymorphic genes, including genes that code for enzymes in the folate and purine pathways. We also included discovery of polymorphic forms of genes that code for enzymes that are inhibited by tungsten: xanthine dehydrogenase, sulfite oxidase (SUOX gene), and aldehyde oxidase. PARTICIPANTS: Eleven case children were age- and sex-matched with 42 community comparison children for genetic analyses. Twenty parents of case children also contributed to the analyses. RESULTS: One bilalleleic gene locus in SUOX was significantly associated with either case or comparison status, depending on which alleles the child carried (without adjusting for multiple comparisons). CONCLUSIONS: Although genetic studies did not provide evidence that a common agent or genetic susceptibility factor caused the leukemias, the association between a SUOX gene locus and disease status in the presence of high tungsten and arsenic levels warrants further investigation. RELEVANCE: Although analyses of community clusters of cancer have rarely identified causes, these findings have generated hypotheses to be tested in subsequent studies. [ABSTRACT FROM AUTHOR]

Context: Population-based estimates of the prevalence of disease-associated mutations, such as hemochromatosis (HFE) gene mutations, are needed to determine the usefulness of genetic screening.Objective: To estimate the prevalence of the HFE mutations C282Y and H63D in the US population.Design: Cross-sectional population-based study of samples in the DNA bank from phase 2 of the Third National Health and Nutrition Examination Survey conducted from 1992 to 1994.Setting and Participants: Genotyped samples of cells from a total of 5171 participants, cross-classified by sex, age, and race/ethnicity in the analysis.Main Outcome Measures: Estimates of the prevalence of C282Y and H63D mutations.Results: The prevalence of C282Y homozygosity is estimated to be 0.26% (95% confidence interval [CI], 0.12%-0.49%); 1.89% (95% CI, 1.48%-2.43%) for H63D homozygosity; and 1.97% (95% CI, 1.54%-2.49%) for compound heterozygosity. The prevalence estimates for C282Y heterozygosity (C282Y/wild type) are 9.54% among non-Hispanic whites, 2.33% among non-Hispanic blacks, and 2.75% among Mexican-Americans. The prevalence estimates of the C282Y mutation in the US population are 5.4% (95% CI, 4.7%-6.2%) and 13.5% (95% CI, 12.5%-14.8%) for the H63D mutation.Conclusions: Estimates of prevalence of HFE mutations are within the expected range for non-Hispanic whites and blacks but the estimated prevalence of the C282Y mutation among Mexican-Americans is less than expected. Mutation data now need to be linked to clinically relevant indices, such as transferrin saturation level. [ABSTRACT FROM AUTHOR]

Measures monoester metabolites on commonly used phthalates in human urine samples in the United States. Use of samples from the National Health and Nutrition Examination Survey; Impact on animal reproductive and developmental toxicology; Sources of contamination; Causes of MBP glucoronidation differences; List of metabolites measured.

Investigates the health effects of 2,3,7,8-tetrachlorodibenzodioxin contaminations in Missouri. Presymptomatic effects in organ systems of persons at risk of exposure; Lack of indications of increased disease prevalence related to putative exposure; Need for the public health policy to concentrate on the prevention of health effects.

Abstract: Humans are exposed to many environmental chemicals, some of which can potentially affect neurodevelopment. Fetuses, infants, and young children are the most susceptible to the effects of these chemicals. As part of the National Health and Examination Survey, 1999–2000, the Centers for Disease Control and Prevention analyzed biological samples for many of these chemicals in a representative sampling of the U.S. population. Concentration data of selected metals, persistent organic pollutants, organophosphorus and carbamate insecticides, and cotinine are presented. For example, the 95th percentile estimates for serum total PCBs (whole weight) in the population aged 20 years and older is about 2.7ng/g. The 95th percentile estimates for serum dioxin total toxic equivalence in the U.S. population aged 20 years and older is between 40 and 50pg/g lipid basis. In general, human levels of these chemicals are decreasing over time in the U.S. population. This reflects the effects of legislation, industry efforts, and changes in lifestyle/activity patterns in the U.S. population. These data will continue to be collected in 2-year cycles and thus allow changes in human levels to be followed. [Copyright &y& Elsevier]

Abstract: Protecting public health from environmental exposures requires four steps: detection of exposures known or expected to cause disease, assessment of health risk from exposure, implementation of an exposure intervention, and assurance that the exposure intervention is effective. To prioritize efforts in these four areas one must consider the size of the population affected, the seriousness of health effects, and the availability of cost-effective exposure interventions. Population exposure data is critical to each of these steps for protecting health. Biomonitoring data for the US population is now available to assist public health scientists and physicians in preventing disease from environmental exposures, and it complements that available for levels of chemicals in environmental media. The Second National Report on Human Exposure to Environmental Chemicals provides for the US population serum, blood and urine levels for 116 environmental chemicals over the years 1999 and 2000, with separate analyses by age, sex, and race/ethnicity. This national exposure information identifies which chemicals get into Americans in measurable quantities; determines whether exposure levels are higher among population subgroups; determines how many Americans have levels of chemicals above recognized health threshold levels (for chemicals with such threshold levels); establishes reference ranges that define general population exposure so unusual exposures can be recognized; assesses the effectiveness of public health efforts to reduce population exposure to selected chemicals; and tracks over time trends in US population exposure. Blood lead measurements in the population were important in identifying lead in gasoline as a significant source of human lead exposure and documenting the reduction in blood lead levels in the population as a result of removing lead from gasoline and other products in the United States. Serum cotinine levels in the early 1990s found more widespread exposure to environmental tobacco smoke (ETS) in the United States than previously thought and additional measurements in 1999 and 2000 documented major declines in exposure to ETS as a result of public health actions in the 1990s. A new biomonitoring assessment of the exposure of the US population will be released every 2 years as the “National Report on Human Exposure to Environmental Chemicals.” These reports will include the current 116 chemicals and new chemicals added to monitor priority exposures of the population. [Copyright &y& Elsevier]

We report human serum levels of selected persistent organic pollutants (POPs) categorized by age, sex, and race/ ethnicity from a statistically representative sampling of the U.S. population during 2003 and 2004. The serum levels are for several chemicals listed in the Stockholm Convention on Persistent Organic Pollutants, in the Geneva Convention on Long-Range Transboundary Air Pollution, or in both. Population data for each chemical are described by geometric means and percentiles and are categorized by age, sex, and race/ ethnicity. At the 90th and 95th percentile, the dioxin total toxic equivalency (TEQ), using the 2005 toxic equivalency factors (TEFs) for all persons 12 years of age and older was 30.9 pg/g lipid (95% confidence interval (CI): 28.2-33.9 pg/g lipid) and 37.8 pg/g lipid (95% CI: 35.3-43.4 pg/g lipid), respectively. At both the 90th and 95th percentiles total TEQ increased significantly with increasing age. The population geometric mean (GM) for the total PCB concentration (sum of 35 congeners) for all persons 12 years of age and older was 0.820 ng/g whole-weight (95% CI: 0.782-0.863 ng/g whole-weight) and 134.4 ng/g lipid (95% CI: 128.9-140.0 ng/g lipid). The population 95th percentile for the total PCB concentration for all persons 12 years of age and older was 3.53 ng/g whole-weight (95% CI: 3.23-3.92 ng/g whole-weight) and 531 ng/g lipid (95% CI: 498-570 ng/g lipid). The concentrations of aldrin, endrin, gamma-HCH, and o,p'-DDT were

We developed a gas chromatography isotope-dilution high-resolution mass spectrometry (GC/ID-HRMS) method for measuring 14 polycyclic aromatic hydrocarbon (PAH) metabolites representing seven parent PAHs in 3 mL of urine at low parts-per-trillion levels. PAH levels were determined in urine samples collected in 1999 and 2000 from approximately 2400 participants in the National Health and Nutrition Examination Survey, and, for the first time, reference range values were calculated for these metabolites in the US population. Using this GC/ID-HRMS method, we found detectable concentrations for monohydroxy metabolite isomers of fluorene, phenanthrene, fluoranthene, pyrene, and chrysene, benzo[c]phenanthrene, and benz[a]anthracene. Some monohydroxy metabolite isomers of benzo[c]phenanthrene, chrysene, and benz[a]anthracene exhibited low detection frequencies that did not allow for geometric mean calculations. Our study results enabled us to establish a reference range for the targeted PAHs in the general US population.

Background: Mandatory folic acid fortification of cereal-grain products was introduced in the United States in 1998 to decrease the risk that women will have children with neural tube defects., Objective: The objective was to determine the effect of folic acid fortification on concentrations of serum and red blood cell (RBC) folate, serum vitamin B-12, and plasma total homocysteine (tHcy) and methylmalonic acid (MMA) in the US population., Design: Blood was collected from a nationally representative sample of approximately 7300 participants aged > or = 3 y in the National Health and Nutrition Examination Survey (NHANES) during 1999-2000 and was analyzed for these B vitamin-status indicators. The results were compared with findings from the prefortification survey NHANES III (1988-1994)., Results: The reference ranges (5th-95th percentiles) were 13.1-74.3 nmol/L for serum folate, 347-1167 nmol/L for RBC folate, and 179-738 pmol/L for serum vitamin B-12. For plasma tHcy and MMA, the reference ranges for serum vitamin B-12-replete participants with normal serum creatinine concentrations were 3.2-10.7 mumol/L and 60-210 nmol/L, respectively. The prevalence of low serum folate concentrations (<6.8 nmol/L) decreased from 16% before to 0.5% after fortification. In elderly persons, the prevalence of high serum folate concentrations (>45.3 nmol/L) increased from 7% before to 38% after fortification; 3% had marginally low serum vitamin B-12 concentrations (<148 pmol/L) and 7% had elevated plasma MMA concentrations (>370 nmol/L). Seventy-eight percent of the US population had plasma tHcy concentrations <9 micromol/L., Conclusions: Every segment of the US population appears to benefit from folic acid fortification. Continued monitoring of B vitamin concentrations in the US population is warranted.

Urine samples collected in 1999 and 2000 as part of the National Health and Nutrition Examination Survey (NHANES) were analyzed for 14 monohydroxy polycyclic aromatic hydrocarbons (PAHs), and, for the first time, reference range values were calculated for these metabolites in the US population. Pyrene is a major component of most PAH mixtures and often is used as a surrogate for total PAH exposure. We detected 1-hydroxypyrene (1-OHpyrene), a metabolite of pyrene, in more than 99% of the samples. The overall geometric mean concentration for 1-OHpyrene in the USA was 79.8 ng/l, with a 95% confidence interval (CI) of 69.0-92.2 ng/l. The overall geometric mean creatinine-adjusted urinary 1-OHpyrene levels in the USA was 74.2 ng/g creatinine (0.039 micromol/mol), with a 95% CI of 64.1-85.9 ng/g creatinine (0.034-0.046 micromol/mol). There were no statistically significant differences among age, gender, or race/ethnicity groups. Adult smokers in the USA have urinary 1-OHpyrene levels three times higher than those of non-smokers. This difference was statistically significant. In this paper, we compare the reference range of urinary 1-OHpyrene levels with levels reported from various occupations by other researchers.

We report population-based concentrations, stratified by age, sex, and racial/ethnic groups, of dialkyl phosphate (DAP) metabolites of multiple organophosphorus pesticides. We measured dimethylphosphate (DMP), dimethylthiophosphate (DMTP), dimethyldithiophosphate (DMDTP), diethylphosphate (DEP), diethylthiophosphate (DETP), and diethyldithiophosphate (DEDTP) concentrations in 1,949 urine samples collected in U.S. residents 6-59 years of age during 1999 and 2000 as a part of the ongoing National Health and Nutrition Examination Survey (NHANES). We detected each DAP metabolite in more than 50% of the samples, with DEP being detected most frequently (71%) at a limit of detection of 0.2 microg/L. The geometric means for the metabolites detected in more than 60% of the samples were 1.85 microg/L for DMTP and 1.04 microg/L for DEP. The 95th percentiles for each metabolite were DMP, 13 microg/L; DMTP, 46 microg/L; DMDTP, 19 micro g/L; DEP, 13 microg/L; DETP, 2.2 microg/L; and DEDTP, 0.87 microg/L. We determined the molar sums of the dimethyl-containing and diethyl-containing metabolites; their geometric mean concentrations were 49.4 and 10.5 nmol/L, respectively, and their 95th percentiles were 583 and 108 nmol/L, respectively. These data are also presented as creatinine-adjusted concentrations. Multivariate analyses showed concentrations of DAPs in children 6-11 years of age that were consistently significantly higher than in adults and often higher than in adolescents. Although the concentrations between sexes and among racial/ethnic groups varied, no significant differences were observed. These data will be important in evaluating the impact of organophosphorus pesticide exposure in the U.S. population and the effectiveness of regulatory actions.

The published literature on serum selenium levels in the US population describes studies on small samples that may not be representative of the US population. This analysis provides the first nationally representative serum selenium levels in the US population by age group, sex, race-ethnicity, poverty income ratio (PIR), geographic region, and urban status. The Third National Health and Nutrition Examination Survey (NHANES III) is a national population-based cross-sectional survey with an in-person interview and serum selenium measurements. For the 18,597 persons for whom serum selenium values wereavailable in NHANES III, the mean concentration was 1.58 nmol/L and the median concentration was 1.56 nmol/L. Mean serum selenium levels differed by age group, sex, race ethnicity, PIR, and geographic region. The US population has slight differences in serum selenium levels by demographic factors.