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.

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.

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.

Investigating childhood leukemia in Churchill County, Nevada.

BACKGROUND: Sixteen children diagnosed with acute leukemia between 1997 and 2002 lived in Churchill County, Nevada, at the time of or before their illness. Considering the county population and statewide cancer rate, fewer than two cases would be expected. OBJECTIVES: In March 2001, the Centers for Disease Control and Prevention led federal, state, and local agencies in a cross-sectional, case-comparison study to determine if ongoing environmental exposures posed a health risk to residents and to compare levels of contaminants in environmental and biologic samples collected from participating families. METHODS: Surveys with more than 500 variables were administered to 205 people in 69 families. Blood, urine, and cheek cell samples were collected and analyzed for 139 chemicals, eight viral markers, and several genetic polymorphisms. Air, water, soil, and dust samples were collected from almost 80 homes to measure more than 200 chemicals. RESULTS: The scope of this cancer cluster investigation exceeded any previous study of pediatric leukemia. Nonetheless, no exposure consistent with leukemia risk was identified. Overall, tungsten and arsenic levels in urine and water samples were significantly higher than national comparison values; however, levels were similar among case and comparison groups. CONCLUSIONS: Although the cases in this cancer cluster may in fact have a common etiology, their small number and the length of time between diagnosis and our exposure assessment lessen the ability to find an association between leukemia and environmental exposures. Given the limitations of individual cancer cluster investigations, it may prove more efficient to pool laboratory and questionnaire data from similar leukemia clusters.

Postservice mortality in Vietnam veterans: 30-year follow-up.

BACKGROUND: During the 1980s, the postservice mortality component of the Vietnam Experience Study was conducted to examine the health effects of the Vietnam experience. This study was limited by the relatively short follow-up and the young age of the veterans. Thus, a follow-up mortality investigation on this cohort was undertaken to further assess the impact of the Vietnam experience on chronic conditions. METHODS: Vital status and underlying cause-of-death data on the Vietnam Experience Study cohort (18 313 male US Army veterans) were retrospectively ascertained from the end of the original study through 2000. Cox proportional hazards regression was used to calculate crude and adjusted rate ratios (RRs) for all-cause and cause-specific mortality, comparing Vietnam and non-Vietnam veterans. RESULTS: All-cause mortality was 7% higher in Vietnam vs non-Vietnam veterans during 30-year follow-up (95% confidence interval [CI], 0.97-1.18). The excess mortality among Vietnam veterans was isolated to the first 5 years after discharge from active duty and resulted from an increase in external causes of death (RR, 1.62; 95% CI, 1.16-2.26). Cause-specific analyses revealed no difference in disease-related mortality. Vietnam veterans, however, experienced excess unintentional poisoning (RR, 2.26; 95% CI, 1.12-4.57) and drug-related (RR, 1.70; 95% CI, 1.01-2.86) deaths throughout follow-up. CONCLUSIONS: Vietnam veterans continued to experience higher mortality than non-Vietnam veterans from unintentional poisonings and drug-related causes. Death rates from disease-related chronic conditions, including cancers and circulatory system diseases, did not differ between Vietnam veterans and their peers, despite the increasing age of the cohort (mean age, 53 years) and the longer follow-up (average, 30 years).

National environmental public health tracking program: bridging the information gap.

In January 2001 the Pew Environmental Health Commission called for the creation of a coordinated public health system to prevent disease in the United States by tracking and combating environmental health threats. In response, the Centers for Disease Control and Prevention initiated the Environmental Public Health Tracking (EPHT) Program to integrate three distinct components of hazard monitoring and exposure and health effects surveillance into a cohesive tracking network. Uniform and acceptable data standards, easily understood case definitions, and improved communication between health and environmental agencies are just a few of the challenges that must be addressed for this network to be effective. The nascent EPHT program is attempting to respond to these challenges by drawing on a wide range of expertise from federal agencies, state health and environmental agencies, nongovernmental organizations, and the program's academic Centers of Excellence. In this mini-monograph, we present innovative strategies and methods that are being applied to the broad scope of important and complex environmental public health problems by developing EPHT programs. The data resulting from this program can be used to identify areas and populations most likely to be affected by environmental contamination and to provide important information on the health and environmental status of communities. EPHT will develop valuable data on possible associations between the environment and the risk of noninfectious health effects. These data can be used to reduce the burden of adverse health effects on the American public.

Heat-related mortality during a 1999 heat wave in Chicago.

BACKGROUND: During the summer of 1999, Chicago's second deadliest heat wave of the decade resulted in at least 80 deaths. The high mortality, exceeded only by a 1995 heat wave, provided the opportunity to investigate the risks associated with heat-related deaths and to examine the effectiveness of targeted heat-relieving interventions. METHODS: We conducted a case-control study to determine risk factors for heat-related death. We collected demographic, health, and behavior information for 63 case patients and 77 neighborhood-and-age-matched control subjects and generated odds ratios (ORs) for each potential risk factor. RESULTS: Fifty-three percent of the case patients were aged <65 years, and psychiatric illness was almost twice as common in the younger than the older age group. In the multivariate analysis, the strongest risk factors for heat-related death were living alone (OR=8.1; 95% confidence interval [CI], 1.4-48.1) and not leaving home daily (OR=5.8; 95% CI, 1.5-22.0). The strongest protective factor was a working air conditioner (OR=0.2; 95% CI, 0.1-0.7). Over half (53%) of the 80 decedents were seen or spoken to on the day of or day before their deaths. CONCLUSIONS: A working air conditioner is the strongest protective factor against heat-related death. The relatively younger age of case patients in 1999 may be due to post-1995 interventions that focused on the elderly of Chicago. However, social isolation and advanced age remain important risk factors. Individual social contacts and educational messages targeted toward at-risk populations during heat waves may decrease the number of deaths in these groups.

Dietary intake, physical activity, body mass index, and childhood asthma in the Third National Health And Nutrition Survey (NHANES III).

Childhood asthma may be affected by dietary changes and increased body mass related to a sedentary lifestyle, although the mechanisms are poorly understood. To test this hypothesis, we used data from the National Health and Nutrition Survey (NHANES III) from 1988-1994, including 7,904 children. We analyzed cross-sectional information on body mass index (BMI = weight/height2), physical activity (hr/day viewing television), dietary intake (24-hr recall), and vitamin C intake (60 mg/day). The probability of self-reported asthma or wheezing relating to risk factors was calculated by logistic regression. After controlling for dietary intake, physical activity, and sociodemographic variables, asthma risk was three times higher for children aged 6-16 years in the highest percentiles of BMI (>95th percentile) when compared to children in percentiles 25-49 (OR = 3.44; 95% CI, 1.49-7.96). No increase was observed in children aged 2-5 years. Low vitamin C intake was marginally related to self-reported current wheezing in children aged 6-16 years. Our results show that increased BMI may influence asthma prevalence in children, but further investigation is needed.

A global approach to childhood lead poisoning prevention.

Childhood lead poisoning is an important, preventable environmental disease affecting millions of children around the world. The effects of lead are well known and range from delayed and adversely affected neurodevelopment to severe health outcomes including seizures, coma, and death. This article reviews the childhood effects of lead poisoning, the approach being taken to the problem in the United States, and the obstacles faced by developing nations in dealing with lead exposure. The United States has attacked the childhood lead poisoning problem by attempting to eliminate sources of exposure, including gasoline, solder in water pipes and cans, and industrial emissions. These actions have resulted in a dramatic reduction in the number of children with elevated blood lead levels in the United States over the last two decades. However, many developing countries are just beginning to address the problem. Successful efforts will need to incorporate epidemiologic methods, source identification, enforced regulations, and a long-term government commitment to eliminating lead as a threat to the next generation of children.

Blood lead levels and risk factors for lead poisoning among children in Jakarta, Indonesia.

The phase-out of leaded gasoline began in Jakarta, Indonesia on July 1, 2001. We evaluated mean blood lead levels (BLLs) and the prevalence of elevated BLLs of Jakarta school children and assessed risk factors for lead exposure in these children before the beginning of the phase-out activities. The study involved a population-based, cross-sectional blood lead survey that included capillary blood lead sampling and a brief questionnaire on risk factors for lead poisoning. A cluster survey design was used. Forty clusters, defined as primary schools in Jakarta, and 15 2nd- and 3rd-grade children in each cluster were randomly selected for participation in the study. The average age of children in this study was 8.6 years (range 6-12) and the geometric mean BLL of the children was 8.6 microg/dl (median: 8.6 microg/dl; range: 2.6-24.1 microg/dl) (n=397). Thirty-five percent of children had BLLs > or =10 microg/dl and 2.4% had BLLs > or =20 microg/dl. Approximately one-fourth of children had BLLs 10-14.9 microg/dl. In multivariate models, level of education of the child's primary caregiver, water collection method, home varnishing and occupational recycling of metals, other than lead, by a family member were predictors of log BLLs after adjustment for age and sex. BLLs of children who lived near a highway or major intersection were significantly higher than those of children who lived near a street with little or no traffic when level of education was not included in the model. Water collection method was a significant predictor of BLLs > or =10 microg/dl after adjustment for age and sex. BLLs in children in this study were moderately high and consistent with BLLs of children in other countries where leaded gasoline is used. With the phase-out of leaded gasoline, BLLs of children in Jakarta are expected to rapidly decline as they have in other countries that have phased lead out of gasoline.

Blood lead levels and risk factors for lead poisoning among children in a Mexican smelting community.

The authors evaluated mean blood lead levels (BLLs) and the prevalence of elevated BLLs in children 1-6 yr of age living in Torreón, Mexico, and assessed risk factors for lead exposure in these children. The study involved a simple random sample of households in the area around a local smelter, as well as a 2-stage cluster sample of neighborhoods and households in the remainder of Torreón. The geometric mean BLL of children in this study (N = 367) was 6.0 microg/dl (95% confidence interval [CI] = 5.2, 6.8) (0.29 microM/l [95% CI = 0.25, 0.33]). Twenty percent of the children had BLLs > or = 10 microg/dl (0.48 microM/l), and 5% had BLLs > or = 20 microg/dl (0.97 microM/l). In multivariate analyses, distance from the smelter, amount of income, and education level of the primary caregiver predicted BLLs. In the environmental risk factor subsample (n = 124), dust and soil lead levels were associated with BLLs and distance from the smelter. BLLs in this study were moderately high, but the levels were lower than those in other smelting communities prior to remediation.

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.

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.

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.

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.

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.

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.

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.