Prevalence of Borrelia burgdorferi and Anaplasma phagocytophilum in Ixodes scapularis (Acari: Ixodidae) nymphs collected in managed red pine forests in Wisconsin.

Changes in the structure of managed red pine forests in Wisconsin caused by interacting root- and stem-colonizing insects are associated with increased abundance of the blacklegged tick, Ixodes scapularis Say, in comparison with nonimpacted stands. However, the frequency and variability of the occurrence of tick-borne pathogens in this coniferous forest type across Wisconsin is unknown. Red pine forests were surveyed from 2009 to 2013 to determine the prevalence of Borrelia burgdorferi and Anaplasma phagocytophilum in questing I. scapularis nymphs. Polymerase chain reaction analysis revealed geographical differences in the nymphal infection prevalence (NIP) of these pathogens in red pine forests. In the Kettle Moraine State Forest (KMSF) in southeastern Wisconsin, NIP of B. burgdorferi across all years was 35% (range of 14.5-53.0%). At the Black River State Forest (BRSF) in western Wisconsin, NIP of B. burgdorferi across all years was 26% (range of 10.9-35.5%). Differences in NIP of B. burgdorferi between KMSF and BRSF were statistically significant for 2010 and 2011 and for all years combined (P < 0.05). NIP ofA. phagocytophilum (human agent) averaged 9% (range of 4.6-15.8%) at KMSF and 3% (range of 0-6.4%) at BRSF, and was significantly different between the sites for all years combined (P < 0.05). Differences in coinfection of B. burgdorferi and A. phagocytophilum were not statistically significant between KMSF and BRSF, with an average of 3.4% (range of 1.7-10.5%) and 2.5% (range of 0-5.5%), respectively. In 2013, the density of infected nymphs in KMSF and BRSF was 14 and 30 per 1000m2, respectively, among the highest ever recorded for the state. Differences in the density of nymphs and NIP among sites were neither correlated with environmental factors nor time since tick colonization. These results document significant unexplained variation in tick-borne pathogens between coniferous forests in Wisconsin that warrants further study.

Long-term renal and neurologic outcomes among survivors of diethylene glycol poisoning.

IMPORTANCE: At least 13 medication-associated diethylene glycol (DEG) mass poisonings have occurred since 1937. To our knowledge, this is the first longitudinal study characterizing long-term health outcomes among survivors beyond the acute poisoning period. OBJECTIVE: To characterize renal and neurologic outcomes among survivors of a 2006 DEG mass-poisoning event in Panama for 2 years after exposure. DESIGN, SETTING, AND PARTICIPANTS: This prospective longitudinal study used descriptive statistics and mixed-effects repeated-measures analysis to evaluate DEG-poisoned survivors at 4 consecutive 6-month intervals (0, 6, 12, and 18 months). Case patients included outbreak survivors with a history of (1) ingestion of DEG-contaminated medication, (2) hospitalization for DEG poisoning, and (3) an unexplained serum creatinine level of 1.5 mg/dL or higher (to convert to micromoles per liter, multiply by 88.4) during acute illness or unexplained exacerbation of preexisting end-stage renal disease. MAIN OUTCOMES AND MEASURES: Demographics, mortality, dialysis dependence, renal function, neurologic signs and symptoms, and nerve conduction studies. RESULTS: Of the 32 patients enrolled, 5 (15.6%) died and 1 was lost to follow-up, leaving 26 patients at 18 months. Three (9.4%) missed 1 or more evaluations. The median age was 62 years (range, 15-88 years), and 59.4% were female. Three (9.4%) patients had preexisting renal failure. Enrollment evaluations occurred at a median of 108 days (range, 65-154 days) after acute illness. The median serum creatinine level for the 22 patients who were not dialysis dependent at time 0 was 5.9 mg/dL (range, 1.8-17.1 mg/dL) during acute illness and 1.8 mg/dL (range, 0.9-5.9 mg/dL) at time 0. Among non-dialysis-dependent patients, there were no significant differences in the log of serum creatinine or estimated glomerular filtration rate over time. The number of patients with subjective generalized weakness declined significantly over time (P < .001). A similar finding was observed for any sensory loss (P = .05). The most common deficits at enrollment were bilateral lower extremity numbness in 13 patients (40.6%) and peripheral facial nerve motor deficits in 7 (21.9%). All patients with neurologic deficits at enrollment demonstrated improvement in motor function over time. Among 28 patients (90.3%) with abnormal nerve conduction study findings at enrollment, 10 (35.7%) had motor axonal involvement, the most common primary abnormality. CONCLUSIONS AND RELEVANCE: Neurologic findings of survivors tended to improve over time. Renal function generally improved among non-dialysis-dependent patients between acute illness and the first evaluation with little variability thereafter. No evidence of delayed-onset neurologic or renal disease was observed.

Maternal concentrations of polyfluoroalkyl compounds during pregnancy and fetal and postnatal growth in British girls.

BACKGROUND: Prenatal exposures to polyfluoroalkyl compounds (PFCs) may be associated with adverse changes in fetal and postnatal growth. OBJECTIVE: We explored associations of prenatal serum concentrations of perfluorooctane sulfonate (PFOS), perfluorooctanoate (PFOA), and perfluorohexane sulfonate (PFHxS) with fetal and postnatal growth in girls. METHODS: We studied a sample of 447 singleton girls and their mothers participating in the Avon Longitudinal Study of Parents and Children (ALSPAC). Data on weight and length were obtained at birth and at 2, 9, and 20 months. Serum samples were obtained in 1991-1992, from mothers during pregnancy. We explored associations between prenatal PFC concentrations and weight at birth as well as longitudinal changes in weight-for-age SD scores between birth and 20 months. RESULTS: PFOS (median, 19.6 ng/mL), PFOA (median, 3.7 ng/mL), and PFHxS (median, 1.6 ng/mL) were detected in 100% of samples. On average, girls born to mothers with prenatal concentrations of PFOS in the upper tertile weighed 140 g less [95% confidence interval (CI): -238, -42] at birth than girls born to mothers with concentrations in the lower tertile in adjusted models. Similar patterns were seen for PFOA (-133 g; 95% CI: -237, -30) and PFHxS (-108 g; 95% CI: -206, -10). At 20 months, however, girls born to mothers with prenatal concentrations of PFOS in the upper tertile weighed 580 g more (95% CI: 301, 858) when compared with those in the lower tertile. No differences in weight were found for PFOA and PFHxS. CONCLUSIONS: Girls with higher prenatal exposure to each of the PFCs examined were smaller at birth than those with lower exposure. In addition, those with higher exposure to PFOS were larger at 20 months.

Blood mercury levels among fish consumers residing in areas with high environmental burden.

Mercury is a ubiquitous, persistent toxicant found in the environment. In water, mercury bioaccumulates up the food chain and leads to high concentrations in fish. Consumption of contaminated fish is the major source of exposure to mercury in the US. The objective of this study was to enroll persons living in areas selected by the Environmental Protection Agency (EPA) to have high mercury concentrations and who consume at least 6o z of locally caught fish per week to determine the feasibility of monitoring future trends among a population identified as highly exposed. Blood samples were collected at time of interview and analyzed for mercury. Participants (n=287) were enrolled from North Carolina, Maryland, and South Dakota. Participants reported eating an average of five servings of fish per week. The overall geometric mean for total mercury was 0.75 µg L(-1), with North Carolina having the highest mean level (2.02 µg L(-1)). Overall, 42% of the study population had levels greater than the US geometric mean 0.83 µg L(-1). The number of servings of fish consumed was not found to be associated with blood mercury levels. We were able to identify some persons with elevated mercury concentrations living in areas identified by EPA; however, identifying and monitoring a highly exposed population over time would be challenging.

Comprehensive assessment of maize aflatoxin levels in Eastern Kenya, 2005-2007.

BACKGROUND: Aflatoxin, a potent fungal toxin, contaminates 25% of crops worldwide. Since 2004, 477 aflatoxin poisonings associated with eating contaminated maize have been documented in Eastern Kenya, with a case-fatality rate of 40%. OBJECTIVE: We characterized maize aflatoxin contamination during the high-risk season (April-June) after the major harvests in 2005, 2006 (aflatoxicosis outbreak years), and 2007 (a non-outbreak year). METHODS: Households were randomly selected each year from the region in Kenya where outbreaks have consistently occurred. At each household, we obtained at least one maize sample (n = 716) for aflatoxin analysis using immunoaffinity methods and administered a questionnaire to determine the source (i.e., homegrown, purchased, or relief) and amount of maize in the household. RESULTS: During the years of outbreaks in 2005 and 2006, 41% and 51% of maize samples, respectively, had aflatoxin levels above the Kenyan regulatory limit of 20 ppb in grains that were for human consumption. In 2007 (non-outbreak year), 16% of samples were above the 20-ppb limit. In addition, geometric mean (GM) aflatoxin levels were significantly higher in 2005 (GM = 12.92, maximum = 48,000 ppb) and 2006 (GM = 26.03, maximum = 24,400 ppb) compared with 2007 (GM = 1.95, maximum = 2,500 ppb) (p-value < 0.001). In all 3 years combined, maize aflatoxin levels were significantly higher in homegrown maize (GM = 17.96) when compared with purchased maize (GM = 3.64) or relief maize (GM = 0.73) (p-value < 0.0001). CONCLUSIONS: Aflatoxin contamination is extreme within this region, and homegrown maize is the primary source of contamination. Prevention measures should focus on reducing homegrown maize contamination at the household level to avert future outbreaks.

Incidence of thyroid disease following exposure to polybrominated biphenyls and polychlorinated biphenyls, Michigan, 1974-2006.

Thyroid hormones, which influence body metabolism and development, could be affected by persistent organic pollutants. We sought to examine the relationship between polybrominated biphenyls (PBBs) and polychlorinated biphenyls (PCBs) and thyroid disease. We employed incidence density sampling to perform a nested case control analysis of the Michigan Long-Term PBB Cohort. Cohort members (n=3333) were exposed to PBBs through contaminated cattle feed in 1973-1974 and to PCBs through daily life. Those with detectable serum PBB and PCB concentrations at enrollment were categorized into tertiles of PBB and PCB exposure. Case-patients were cohort members answering "Yes" to "Has a healthcare provider ever told you that you had a thyroid problem?" during follow-up interviews; control-patients were cohort members answering "No". We used odds ratios (OR) with 95% confidence intervals (CI) to compare odds of thyroid disease by PBB and PCB exposure and by various risk factors. Total cumulative thyroid disease incidence after 33 years was 13.9% among women and 2.6% among men. After adjusting for body mass index, we found no statistically significant differences in odds of any type of thyroid disease among women or men with elevated PBB or PCB exposure. Compared to control-patients, women with thyroid disease had increased odds of being overweight/obese (OR=2.82, 95% CI: 1.94-4.11) and developing infertility (OR=1.71, 95% CI: 1.08-2.69), diabetes (OR=1.61, 95% CI: 1.04-2.51), or arthritis (OR=1.71, 95% CI: 1.18-2.50) during follow-up. Additional research should explore potential associations between PBBs/PCBs and thyroid disease among children exposed in utero.

Timing of maturation and predictors of Tanner stage transitions in boys enrolled in a contemporary British cohort.

This study describes the timing of puberty in 8- to 14-year-old boys enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC) and identifies factors associated with earlier achievement of advanced pubic hair stages. Women were enrolled during pregnancy and their offspring were followed prospectively. We analysed self-reported pubic hair Tanner staging collected annually. We used survival models to estimate median age of attainment of pubic hair stage >1, stage >2 and stage >3 of pubic hair development. We also constructed multivariable logistic regression models to identify factors associated with earlier achievement of pubic hair stages. Approximately 5% of the boys reported Tanner pubic hair stage >1 at age 8; 99% of boys were at stage >1 by age 14. The estimated median ages of entry into stages of pubic hair development were 11.4 years [95% confidence interval (CI) 11.3, 11.4] for stage >1, 12.7 years [95% CI 12.7, 12.8] for stage >2 and 13.5 years [95% CI 13.5, 13.6] for stage >3. Predictors of younger age at Tanner stage >1 included low birthweight, younger maternal age at delivery and being taller at age 8. Associations were found between younger age at attainment of stage >2 and gestational diabetes and taller or heavier body size at age 8. Being taller or heavier at age 8 also predicted younger age at Tanner stage >3. The results give added support to the strong influence of pre-adolescent body size on male pubertal development; the tallest and heaviest boys at 8 years achieved each stage earlier and the shortest boys later. Age at attainment of pubic hair Tanner stages in the ALSPAC cohort are similar to ages reported in other European studies that were conducted during overlapping time periods. This cohort will continue to be followed for maturational information until age 17.

Diethylene glycol in health products sold over-the-counter and imported from Asian countries.

Diethylene glycol (DEG), a chemical that has been implicated in multiple medication-associated mass poisonings, can result in renal and neurological toxicity if ingested. Three previous such mass poisonings implicated Chinese manufacturers as the origin of contaminated ingredients. No literature exists on potential DEG or triethylene glycol (TEG), a related compound, contamination of health products imported from Asian countries to the USA. Our primary objective was to quantitatively assess the amount of DEG present in a convenience sampling of these health products. The study's secondary objectives were to: (1) evaluate for, and quantify TEG levels in these samples; (2) compare DEG and TEG levels in these products directly to levels in medications implicated in previous similar mass poisonings; and (3) to estimate DEG dose (in mg/kg) based on the manufacturer's instructions and compare these values to toxic doses from past mass poisonings and the literature. A quantitative assessment of DEG and TEG was performed in a convenience sampling of over-the-counter health products imported from Asian countries. Results were converted to volume to volume (v/v) % and compared with DEG levels in medications implicated in previous mass poisonings. Estimated doses (based on the manufacturer's instructions) of each product with detectable levels of DEG for a 70 kg adult were compared to toxic doses of DEG reported in the literature. Seventeen of 85 (20%) samples were not able to be analyzed for DEG or TEG due to technical reasons. Fifteen of 68 (22%) samples successfully tested had detectable levels of DEG (mean, 18.8 µg/ml; range, 0.791-110.1 µg/ml; and volume to volume (v/v) range, 0.00007-0.01%). Two of 68 (3%) samples had TEG levels of 12.8 and 20.2 µg/ml or 0.0012% and 0.0018% TEG v/v. The product with the highest DEG% by v/v was 810 times less than the product involved in the Panama DEG mass poisoning (8.1%). The lowest reported toxic dose from a past DEG mass poisoning (14 mg/kg) was more than 150 times higher than the highest daily dose estimated in our study (0.09 mg/kg). Sixty-eight of 85 (80%) samples were able to be successfully analyzed for DEG and TEG. DEG and TEG were detectable in 15/68 (22%) and 2/68 (3%) samples, respectively. Based on current standards, these levels probably do not represent an acute public health threat. Additional research focusing on why DEG is found in these products and on the minimum amount of DEG needed to result in toxicity is needed.

Exposure to polyfluoroalkyl chemicals during pregnancy is not associated with offspring age at menarche in a contemporary British cohort.

INTRODUCTION: Polyfluoroalkyl chemicals (PFCs) are commercially synthesized chemicals used in consumer products. Exposure to certain PFCs is widespread, and some PFCs may act as endocrine disruptors. We used data from the Avon Longitudinal Study of Parents and Children (ALSPAC) in the United Kingdom to conduct a nested case-control study examining the association between age at menarche, and exposure to PFCs during pregnancy. METHODS: Cases were selected from female offspring in the ALSPAC who reported menarche before the age of 11.5 years (n = 218), and controls were a random sample of remaining girls (n = 230). Serum samples taken from the girls' mothers during pregnancy (1991-1992) were analyzed using on-line solid-phase extraction coupled to isotope dilution high-performance liquid chromatography-tandem mass spectrometry for 8 PFCs. Logistic regression was used to determine association between maternal serum PFC concentrations, and odds of earlier age at menarche. RESULTS: PFOS and PFOA were the predominant PFCs (median serum concentrations of 19.8 ng/mL and 3.7 ng/mL). All but one PFC were detectable in most samples. Total PFC concentration varied by number of births (inverse association with birth order; p-value < 0.0001) and race of the child (higher among whites; p-value = 0.03). The serum concentrations of carboxylates were associated with increased odds of earlier age at menarche; concentrations of perfluorooctane sulfonamide, the sulfonamide esters and sulfonates were all associated with decreased odds of earlier age at menarche. However, all confidence intervals included the null value of 1.0. CONCLUSIONS: ALSPAC study participants had nearly ubiquitous exposure to most PFCs examined, but PFC exposure did not appear to be associated with altered age at menarche of their offspring.

Progression through puberty in girls enrolled in a contemporary British cohort.

PURPOSE: Patterns of pubertal development reflect underlying endocrine function and exposures, and could affect future health outcomes. We used data from a longitudinal cohort to describe factors associated with breast and pubic hair stage and estimate average duration of puberty. METHODS: Data from the Avon Longitudinal Study of Parents and Children were used to describe timing and duration of pubertal development in girls. Self-reported Tanner stage of breast and pubic hair and menarche status were collected from ages 8-14 through mailed questionnaires. Factors associated with breast and pubic hair stage were identified using ordinal probit models. Age at entry into breast and pubic hair stages, and duration of puberty were estimated using interval-censored parametric survival analysis. RESULTS: Among the 3,938 participants, being overweight or obese, of non-white race, being the firstborn, and younger maternal age at menarche were associated with more advanced breast and pubic hair stages. Having an overweight or obese mother was associated with more advanced breast stages. Time spent in breast stages 2 and 3 was longer (1.5 years) than time spent in pubic hair stages 2 and 3 (1 year). The average age at menarche was 12.9 (95% CI, 12.8-12.9) years, and average duration of puberty (time from initiation of puberty to menarche) was 2.7 years. CONCLUSIONS: Girls in Avon Longitudinal Study of Parents and Children had a slightly longer duration of puberty compared to an earlier British cohort study. Various maternal and child characteristics were associated with breast and pubic hair stage, including both child and maternal body mass.

Role of prenatal characteristics and early growth on pubertal attainment of British girls.

OBJECTIVES: The objective of this study was to explore the influence of maternal prenatal characteristics and behaviors and of weight and BMI gain during early childhood on the timing of various puberty outcomes in girls who were enrolled in the Avon Longitudinal Study of Parents and Children. METHODS: Repeated self-assessments of pubertal development were obtained from approximately 4000 girls between the ages of 8 and 14. Data on prenatal characteristics and weight at birth and 2, 9, and 20 months of age were obtained from questionnaires, birth records, and clinic visits. Infants' weights were converted to weight-for-age and BMI SD scores (SDSs; z scores), and change values were obtained for the 0- to 20-month and other intervals within that age range. We used parametric survival models to estimate associations with age of entry into Tanner stages of breast and pubic hair and menarche. RESULTS: Maternal initiation of menarche at age<12, smoking during pregnancy, and primiparity were associated with earlier puberty. A 1-unit increase in the weight SDS change values for the 0- to 20-month age interval was associated with earlier ages of entry into pubertal outcomes (0.19-0.31 years). Increases in the BMI SDS change values were also associated with earlier entry into pubertal outcomes (0.07-0.11 years). CONCLUSIONS: Many of the maternal prenatal characteristics and weight and BMI gain during infancy seemed to have similar influences across different puberty outcomes. Either such early factors have comparable influences on each of the hormonal processes involved in puberty, or processes are linked and awakening of 1 aspect triggers the others.

Pubertal pathways in girls enrolled in a contemporary british cohort.

Data from the Avon Longitudinal Study of Parents and Children were used to describe initiation of secondary sexual characteristic development of girls. Tanner stages of breast and pubic hair and menarche status were self-reported via mailed questionnaires, administered from ages 8-14. Initiation pathway was categorized as breast [thelarche] or pubic hair [pubarche] development alone, or synchronous. Average ages at beginning breast and pubic hair development were estimated using survival analysis. Factors associated with initiation pathway were assessed using logistic regression. Among the 3938 participants, the median ages at beginning breast and pubic hair development were 10.19 (95% CI: 10.14-10.24) and 10.95 (95% CI: 10.90-11.00) years. Synchronous initiation was the most commonly reported pathway (46.3%), followed by thelarche (42.1%). Girls in the pubarche pathway were less likely to be obese or overweight at age 8 or have an overweight or obese mother. Girls in the thelarche pathway were less likely to be of nonwhite race or be the third born or later child.

Public health partnerships in medical toxicology education and practice.

In December 2002, the medical toxicology sub-board, which consists of representatives from emergency medicine, preventive medicine, and pediatrics, released revised core content for medical toxicology, aiming to better meet the academic challenges imposed by the continually expanding knowledge base of medical toxicology. These challenges included the addition of relatively new areas of interest in medical toxicology, including population health, while simultaneously ensuring that a structural framework existed to accommodate future areas of interest. There is no evidence readily available to assess how well the educational curricula of existing fellowship programs are meeting these needs. In an effort to address this, the authors describe a medical toxicology fellowship program that consists of a partnership among the Emory University School of Medicine, the Georgia Poison Control Center, and the CDC, as well as the results of a reorganization of its academic curriculum that occurred in 2006. To the best of the authors' knowledge, this is the first published report describing such a curriculum redesign. Suggestions and potential resources proposed as enhancements for the public health-associated education of medical toxicology fellows are discussed. The authors also seek to initiate a discussion among programs about how to optimally meet the new challenges developed by the medical toxicology sub-board.

Investigation of sex differences in hip structure in peripubertal children.

CONTEXT: There is evidence that sex differences in hip structure are increased during puberty, possibly as a consequence of associated changes in body composition. OBJECTIVES: The objective of the study was to explore relationships between sex, puberty, hip structure, and body composition. DESIGN/SETTING: The design was a longitudinal birth cohort study: The Avon Longitudinal Study of Parents and Children. PARTICIPANTS: Participants included 3914 boys and girls (mean age 13.8 yr). OUTCOME MEASURES: Measures included dual-energy x-ray absorptiometry-derived femoral neck width (FNW), cortical thickness (CT), bending strength [cross-sectional moment of inertia (CSMI)], section modulus, buckling ratio (BR), and femoral neck and total hip bone mineral density. RESULTS: FNW, CT, and CSMI were higher in boys, whereas BR was lower in girls (P<0.001). Differences in hip structure were studied according to puberty (self-completion Tanner stage questionnaires). FNW, CT, and CSMI were higher in Tanner stage IV/V vs. I/II, particularly in boys (P<0.001, puberty-sex interaction). BR was lower in Tanner stage IV/V, particularly in girls (P=0.008, puberty-sex interaction). Adjusting for height, fat mass, and lean mass resulted in differential attenuation in the sexes, such that CT attenuated by about 80% and about 40% in boys and girls, respectively (P=0.004, puberty-sex interaction for adjusted CT, Tanner stages I/II vs. IV/V). The difference in BR showed little attenuation after adjustment. CONCLUSION: During puberty, hip-bending strength increases, particularly in boys, due to their greater FNW, reflecting changes in height, fat mass, and lean mass. In contrast, BR falls during puberty, particularly in girls, reflecting their smaller FNW relative to CT, involving mechanisms partly independent of height and body composition.

Characterization of the correlation between ages at entry into breast and pubic hair development.

PURPOSE: The timing of breast and pubic hair development in girls are related, but the degree of correlation has not been well characterized. Periodic observations also are complicated by interval censoring. METHODS: Data used were from the Avon Longitudinal Study of Parents and Children. Mean age at entry into breast and pubic hair development was determined by the use of parametric survival analysis. The bivariate normal cumulative distribution function was evaluated over the region containing the paired event times; the likelihood was maximized with respect to the correlation coefficient rho. RESULTS: Among 3938 participants, estimated mean ages at entry into Tanner stage 2 for breast and pubic hair development were 10.19 and 10.95, respectively. The likelihood was maximized at rho = 0.503 to 0.506. This value remained relatively constant among subgroups, although some heterogeneity was observed by maternal and child body mass index and birth order. CONCLUSIONS: The timing of breast and of pubic hair development is moderately correlated and remain so when it is stratified by characteristics associated with puberty.

Postmortem blood cadmium, lead, and mercury concentrations: comparisons with regard to sampling location and reference ranges for living persons.

This study's goal was to determine cadmium (Cd), lead (Pb), total mercury (THg), and inorganic mercury (IHg) levels in human cadavers to compare measured levels with established reference ranges for living persons and to determine whether blood levels varied with time from death to sample collection or by body collection site. Subjects (n = 66) recruited from the Fulton County Medical Examiner's Office in Atlanta, GA, were 20 years of age or older, had no penetrating trauma, no obvious source of environmental contamination of the vasculature, and had whole blood accessible from the femoral (F) site, the cardiac (C) site, or both. Geometric mean results were as follows: 2.59 microg/L F-Cd; 11.81 microg/L C-Cd; 1.03 microg/L F-THg; 2.01 microg/L C-THg; 0.29 microg/L F-IHg; 0.49 microg/L C-IHg; 1.78 microg/dL F-Pb; and 1.87 microg/dL C-Pb. Both F- and C-Cd levels as well as C-THg levels were significantly higher than reference values among living persons (C- and F-Cd, p < 0.0001 and C-THg, p = 0.0001, respectively). Based on regression modeling, as the postmortem interval increased, blood Cd levels increased (p < 0.006). Postmortem blood Cd concentrations were elevated compared to population values and varied with respect to sampling location and postmortem interval.

Medication-associated diethylene glycol mass poisoning: a review and discussion on the origin of contamination.

Diethylene glycol (DEG), an extremely toxic chemical, has been implicated as the etiologic agent in at least 12 medication-associated mass poisonings over the last 70 years. Why DEG mass poisonings occur remains unclear. Most reports do not contain detailed reports of trace-back investigations into the etiology. The authors, therefore, conducted a systematic literature review on potential etiologies of these mass poisonings. The current available evidence suggests that substitution of DEG or DEG-containing compounds for pharmaceutical ingredients results from: (1) deception as to the true nature of certain ingredients by persons at some point in the pharmaceutical manufacturing process, and (2) failure to adhere to standardized quality control procedures in manufacturing pharmaceutical products intended for consumers. We discuss existing guidelines and new recommendations for prevention of these incidents.

Genetic variation in LIN28B is associated with the timing of puberty.

The timing of puberty is highly variable. We carried out a genome-wide association study for age at menarche in 4,714 women and report an association in LIN28B on chromosome 6 (rs314276, minor allele frequency (MAF) = 0.33, P = 1.5 × 10(-8)). In independent replication studies in 16,373 women, each major allele was associated with 0.12 years earlier menarche (95% CI = 0.08-0.16; P = 2.8 × 10(-10); combined P = 3.6 × 10(-16)). This allele was also associated with earlier breast development in girls (P = 0.001; N = 4,271); earlier voice breaking (P = 0.006, N = 1,026) and more advanced pubic hair development in boys (P = 0.01; N = 4,588); a faster tempo of height growth in girls (P = 0.00008; N = 4,271) and boys (P = 0.03; N = 4,588); and shorter adult height in women (P = 3.6 × 10(-7); N = 17,274) and men (P = 0.006; N = 9,840) in keeping with earlier growth cessation. These studies identify variation in LIN28B, a potent and specific regulator of microRNA processing, as the first genetic determinant regulating the timing of human pubertal growth and development.

Summary and findings of the EPA and CDC symposium on air pollution exposure and health.

The U.S. Environmental Protection Agency (EPA) and the U.S. Centers for Disease Control (CDC) co-organized a symposium on "Air Pollution Exposure and Health" at Research Triangle Park, North Carolina on September 19-20, 2006. The symposium brought together health and environmental scientists to discuss the state of the science and the cross-jurisdictional and methodological challenges in conducting air pollution epidemiology, environmental public health tracking and accountability research. The symposium was held over 2 days and consisted of technical presentations and breakout group discussions on each of the three principal themes of this meeting: (1) monitoring and exposure modeling information, (2) health effects data and (3) linkage of air quality and health data for research, tracking and accountability. This paper summarizes the symposium presentations and the conclusions and recommendations developed during the meeting. The accompanying two papers, which appear in this issue of the Journal, provide more in-depth discussion of issues pertinent to obtaining and analyzing air pollution exposure and health information. The symposium succeeded in identifying areas where there are critical gaps of knowledge in existing air pollution exposure and health information and in discovering institutional or programmatic barriers, which impede accessing and linking disparate data sets. Several suggestions and recommendations emerged from this meeting, directed toward (1) improving the utility of air monitoring data for exposure quantification, (2) improving access to and the quality of health data, (3) studying emerging air quality and health issues, (4) exploring improved or novel methods for linking data and (5) developing partnerships, building capacity and facilitating interdisciplinary communication. The meeting was successful in promoting an interdisciplinary dialogue around these issues and in formulating strategies to support these recommended activities. Finally, this symposium subsequently led to strengthening and initiating new partnerships or interactions between the EPA, CDC, States, academia and the research community at large.