Stephanie Kieszak

Aflatoxin contamination of commercial maize products during an outbreak of acute aflatoxicosis in eastern and central Kenya.

In April 2004, one of the largest aflatoxicosis outbreaks occurred in rural Kenya, resulting in 317 cases and 125 deaths. Aflatoxin-contaminated homegrown maize was the source of the outbreak, but the extent of regional contamination and status of maize in commercial markets (market maize) were unknown. We conducted a cross-sectional survey to assess the extent of market maize contamination and evaluate the relationship between market maize aflatoxin and the aflatoxicosis outbreak. We surveyed 65 markets and 243 maize vendors and collected 350 maize products in the most affected districts. Fifty-five percent of maize products had aflatoxin levels greater than the Kenyan regulatory limit of 20 ppb, 35% had levels > 100 ppb, and 7% had levels > 1,000 ppb. Makueni, the district with the most aflatoxicosis case-patients, had significantly higher market maize aflatoxin than did Thika, the study district with fewest case-patients (geometric mean aflatoxin = 52.91 ppb vs. 7.52 ppb, p = 0.0004). Maize obtained from local farms in the affected area was significantly more likely to have aflatoxin levels > 20 ppb compared with maize bought from other regions of Kenya or other countries (odds ratio = 2.71; 95% confidence interval, 1.12–6.59). Contaminated homegrown maize bought from local farms in the affected area entered the distribution system, resulting in widespread aflatoxin contamination of market maize. Contaminated market maize, purchased by farmers after their homegrown supplies are exhausted, may represent a source of continued exposure to aflatoxin. Efforts to successfully interrupt exposure to aflatoxin during an outbreak must consider the potential role of the market system in sustaining exposure.

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

BACKGROUND During the summer of 1999, Chicagos 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.

Case-control study of an acute aflatoxicosis outbreak, Kenya, 2004

Objectives: During January–June 2004, an aflatoxicosis outbreak in eastern Kenya resulted in 317 cases and 125 deaths. We conducted a case–control study to identify risk factors for contamination of implicated maize and, for the first time, quantitated biomarkers associated with acute aflatoxicosis. Design: We administered questionnaires regarding maize storage and consumption and obtained maize and blood samples from participants. Participants: We recruited 40 case-patients with aflatoxicosis and 80 randomly selected controls to participate in this study. Evaluations/Measurements: We analyzed maize for total aflatoxins and serum for aflatoxin B1–lysine albumin adducts and hepatitis B surface antigen. We used regression and survival analyses to explore the relationship between aflatoxins, maize consumption, hepatitis B surface antigen, and case status. Results: Homegrown (not commercial) maize kernels from case households had higher concentrations of aflatoxins than did kernels from control households [geometric mean (GM) = 354.53 ppb vs. 44.14 ppb; p = 0.04]. Serum adduct concentrations were associated with time from jaundice to death [adjusted hazard ratio = 1.3; 95% confidence interval (CI), 1.04–1.6]. Case patients had positive hepatitis B titers [odds ratio (OR) = 9.8; 95% CI, 1.5–63.1] more often than controls. Case patients stored wet maize (OR = 3.5; 95% CI, 1.2–10.3) inside their homes (OR = 12.0; 95% CI, 1.5–95.7) rather than in granaries more often than did controls. Conclusion: Aflatoxin concentrations in maize, serum aflatoxin B1–lysine adduct concentrations, and positive hepatitis B surface antigen titers were all associated with case status. Relevance: The novel methods and risk factors described may help health officials prevent future outbreaks of aflatoxicosis.

Heat-related death and mental illness during the 1999 Cincinnati heat wave.

During a 1999 heat wave in Cincinnati, Ohio, the Hamilton County Coroner reported 18 heat-related deaths. The Centers for Disease Control and Prevention and the Cincinnati Department of Health conducted a case–control study using surrogate case information and first-person control information to identify risk factors for mortality during the heat wave. Surrogate data were supplemented by systematic death scene investigation reports and comprehensive toxicologic screens, important sources of data that are routinely collected by the Hamilton County Coroner’s Office. The study included 17 case subjects and 34 controls from the decedents’ neighborhood. Among 17 case subjects, 8 (47.1%) had mental illness (odds ratio [OR], 14.0; 95% confidence interval [CI], 1.8–633). There was a suggestion of an interaction between age and mental health. A working air-conditioner was the strongest protective factor (OR, 0.03; 95% CI, 0–0.2). Toxicologic screening indicated that case subjects with reported mental illness and a prescription for psychotropic drugs may not have been medication compliant. Three decedents lived in group homes for people with mental illness, indicating that opportunities for prevention may have been missed. Systematic death investigations, including toxicologic screening, provide valuable information about the circumstances of heat-related death, particularly the role of medication compliance as a risk factor. Prevention programs during heat waves should target people with mental illness, especially those who take psychotropic medication.

Recreational exposure to microcystins during algal blooms in two California lakes.

We conducted a study of recreational exposure to microcystins among 81 children and adults planning recreational activities on either of three California reservoirs, two with significant, ongoing blooms of toxin-producing cyanobacteria, including Microcystis aeruginosa (Bloom Lakes), and one without a toxin-producing algal bloom (Control Lake). We analyzed water samples for algal taxonomy, microcystin concentrations, and potential respiratory viruses (adenoviruses and enteroviruses). We measured microcystins in personal air samples, nasal swabs, and blood samples. We interviewed study participants for demographic and health symptoms information. We found highly variable microcystin concentrations in Bloom Lakes (<10 microg/L to >500 microg/L); microcystin was not detected in the Control Lake. We did not detect adenoviruses or enteroviruses in any of the lakes. Low microcystin concentrations were found in personal air samples (<0.1 ng/m(3) [limit of detection]-2.89 ng/m(3)) and nasal swabs (<0.1 ng [limit of detection]-5 ng). Microcystin concentrations in the water-soluble fraction of all plasma samples were below the limit of detection (1.0 microg/L). Our findings indicate that recreational activities in water bodies that experience toxin-producing cyanobacterial blooms can generate aerosolized cyanotoxins, making inhalation a potential route of exposure. Future studies should include collecting nasal swabs to assess upper respiratory tract deposition of toxin-containing aerosols droplets.

Stature and pubertal stage assessment in American boys: the 1988-1994 Third National Health and Nutrition Examination Survey.

PURPOSE To describe current stature and pubertal development in North American boys, and to compare these measures with measures observed approximately 30 years ago. METHODS We analyzed data (i.e., height, weight, and Tanner Stage) from the Third National Health and Nutrition Examination Survey (NHANES III), conducted between 1988-1994, and compared it to the National Health Examination Survey, Cycles II and III (HES II/III), conducted from 1963-1965 and 1966-1970. The surveys included physical examination and questionnaire components, employed cross-sectional designs, and are nationally representative. We used logistic regression to calculate median age at onset of pubertal stages. RESULTS NHANES III included 2481 boys aged 8 to 18 years. HES II comprised 3010 boys aged 8-11 years and HES III comprised 3514 boys aged 12-17 years. The mean heights of the oldest boys in both surveys did not differ significantly; however, at younger ages, boys in the more recent survey were taller (average height difference among those aged 8-14 years was 2.0 cm). Boys in NHANES III were also heavier and had higher body mass index than those in HES II/III. The median estimated ages of onset of pubertal stages in NHANES III were 9.9, 12.2, 13.6, and 15.8 years for genital stages 2-5, respectively, and 11.9, 12.6, 13.6, and 15.7 years for pubic hair stages 2-5, respectively. For some stages, the median estimated age of onset of puberty was earlier among boys in NHANES III than among those in HES III. CONCLUSIONS Differences in mean height at young ages, but not at older ages, suggest that the rate of growth among boys in NHANES III was faster than that of boys in the earlier surveys. This finding, coupled with the finding of earlier ages of onset of some pubertal stages, suggests that boys of this generation may be maturing more rapidly than did boys in the past.

Timing of maturation and predictors of menarche in girls enrolled in a contemporary British cohort

This study describes the timing of puberty in 8- to 13-year-old girls enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC) and identifies factors associated with earlier achievement of menarche. Women were enrolled during pregnancy and their offspring were followed prospectively. We analysed self-reported Tanner staging and menstrual status information collected annually from daughters up to age 13. We used survival models to estimate median age of attainment of stage >1 and stage >2 of breast and pubic hair development and of menarche. We also constructed multivariable logistic regression models to identify factors associated with earlier achievement of menarche. About 12% of girls reported Tanner breast stage >1 at age 8; 98% of girls were above stage 1 by age 13. For pubic hair, 5% and 95% of girls had attained a stage >1 by 8 and 13 years, respectively. The estimated median age of entry into stage >1 of breast development was 10.14 years (95% confidence interval [CI], 10.08, 10.19), and for pubic hair development the median age was 10.92 years [95% CI, 10.87, 10.97]. One girl (out of 2953) had attained menarche by age 8; 60% had attained menarche by age 13. The estimated median age at menarche was 12.93 years [95% CI, 12.89, 12.98]. Prenatal predictors of menarche by age 11 (12% of girls) included earlier maternal age at menarche, high maternal pre-pregnancy body mass index, smoking during the third trimester, and non-white race; the single postnatal predictor was the girls body size at 8 years. Age at attainment of breast and pubic hair Tanner stage and age at menarche in the ALSPAC cohort are similar to ages reported in other European studies that were conducted during overlapping time periods. The results also give added support to the strong influence of maternal maturation, pre-adolescent body size and race on the timing of a girls menarche. This cohort will continue to be followed for maturational information until age 17.

Serum selenium levels in the US population: Third National Health and Nutrition Examination Survey, 1988-1994.

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 were available in NHANES III, the mean concentration was 1.58 µmol/L and the median concentration was 1.56 µmol/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.

Recreational exposure to low concentrations of microcystins during an algal bloom in a small lake.

We measured microcystins in blood from people at risk for swallowing water or inhaling spray while swimming, water skiing, jet skiing, or boating during an algal bloom. We monitored water samples from a small lake as a Microcystis aeruginosa bloom developed. We recruited 97 people planning recreational activities in that lake and seven others who volunteered to recreate in a nearby bloom-free lake. We conducted our field study within a week of finding a 10-μg/L microcystin concentration. We analyzed water, air, and human blood samples for water quality, potential human pathogens, algal taxonomy, and microcystin concentrations. We interviewed study participants for demographic and current health symptom information. Water samples were assayed for potential respiratory viruses (adenoviruses and enteroviruses), but none were detected. We did find low concentrations of Escherichia coli, indicating fecal contamination. We found low levels of microcystins (2 μg/L to 5 μg/L) in the water and (<0.1 ng/m3) in the aerosol samples. Blood levels of microcystins for all participants were below the limit of detection (0.147μg/L). Given this low exposure level, study participants reported no symptom increases following recreational exposure to microcystins. This is the first study to report that water-based recreational activities can expose people to very low concentrations of aerosol-borne microcystins; we recently conducted another field study to assess exposures to higher concentrations of these algal toxins.

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.