Margaret Kurzius-Spencer

Prevalence and Characteristics of Autism Spectrum Disorder Among Children Aged 8 Years--Autism and Developmental Disabilities Monitoring Network, 11 Sites, United States, 2012

PROBLEM/CONDITION Autism spectrum disorder (ASD). PERIOD COVERED 2012. DESCRIPTION OF SYSTEM The Autism and Developmental Disabilities Monitoring (ADDM) Network is an active surveillance system that provides estimates of the prevalence and characteristics of ASD among children aged 8 years whose parents or guardians reside in 11 ADDM Network sites in the United States (Arkansas, Arizona, Colorado, Georgia, Maryland, Missouri, New Jersey, North Carolina, South Carolina, Utah, and Wisconsin). Surveillance to determine ASD case status is conducted in two phases. The first phase consists of screening and abstracting comprehensive evaluations performed by professional service providers in the community. Data sources identified for record review are categorized as either 1) education source type, including developmental evaluations to determine eligibility for special education services or 2) health care source type, including diagnostic and developmental evaluations. The second phase involves the review of all abstracted evaluations by trained clinicians to determine ASD surveillance case status. A child meets the surveillance case definition for ASD if one or more comprehensive evaluations of that child completed by a qualified professional describes behaviors that are consistent with the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision diagnostic criteria for any of the following conditions: autistic disorder, pervasive developmental disorder-not otherwise specified (including atypical autism), or Asperger disorder. This report provides ASD prevalence estimates for children aged 8 years living in catchment areas of the ADDM Network sites in 2012, overall and stratified by sex, race/ethnicity, and the type of source records (education and health records versus health records only). In addition, this report describes the proportion of children with ASD with a score consistent with intellectual disability on a standardized intellectual ability test, the age at which the earliest known comprehensive evaluation was performed, the proportion of children with a previous ASD diagnosis, the specific type of ASD diagnosis, and any special education eligibility classification. RESULTS For 2012, the combined estimated prevalence of ASD among the 11 ADDM Network sites was 14.6 per 1,000 (one in 68) children aged 8 years. Estimated prevalence was significantly higher among boys aged 8 years (23.6 per 1,000) than among girls aged 8 years (5.3 per 1,000). Estimated ASD prevalence was significantly higher among non-Hispanic white children aged 8 years (15.5 per 1,000) compared with non-Hispanic black children (13.2 per 1,000), and Hispanic (10.1 per 1,000) children aged 8 years. Estimated prevalence varied widely among the 11 ADDM Network sites, ranging from 8.2 per 1,000 children aged 8 years (in the area of the Maryland site where only health care records were reviewed) to 24.6 per 1,000 children aged 8 years (in New Jersey, where both education and health care records were reviewed). Estimated prevalence was higher in surveillance sites where education records and health records were reviewed compared with sites where health records only were reviewed (17.1 per 1,000 and 10.7 per 1,000 children aged 8 years, respectively; p<0.05). Among children identified with ASD by the ADDM Network, 82% had a previous ASD diagnosis or educational classification; this did not vary by sex or between non-Hispanic white and non-Hispanic black children. A lower percentage of Hispanic children (78%) had a previous ASD diagnosis or classification compared with non-Hispanic white children (82%) and with non-Hispanic black children (84%). The median age at earliest known comprehensive evaluation was 40 months, and 43% of children had received an earliest known comprehensive evaluation by age 36 months. The percentage of children with an earliest known comprehensive evaluation by age 36 months was similar for boys and girls, but was higher for non-Hispanic white children (45%) compared with non-Hispanic black children (40%) and Hispanic children (39%). INTERPRETATION Overall estimated ASD prevalence was 14.6 per 1,000 children aged 8 years in the ADDM Network sites in 2012. The higher estimated prevalence among sites that reviewed both education and health records suggests the role of special education systems in providing comprehensive evaluations and services to children with developmental disabilities. Disparities by race/ethnicity in estimated ASD prevalence, particularly for Hispanic children, as well as disparities in the age of earliest comprehensive evaluation and presence of a previous ASD diagnosis or classification, suggest that access to treatment and services might be lacking or delayed for some children. PUBLIC HEALTH ACTION The ADDM Network will continue to monitor the prevalence and characteristics of ASD among children aged 8 years living in selected sites across the United States. Recommendations from the ADDM Network include enhancing strategies to 1) lower the age of first evaluation of ASD by community providers in accordance with the Healthy People 2020 goal that children with ASD are evaluated by age 36 months and begin receiving community-based support and services by age 48 months; 2) reduce disparities by race/ethnicity in identified ASD prevalence, the age of first comprehensive evaluation, and presence of a previous ASD diagnosis or classification; and 3) assess the effect on ASD prevalence of the revised ASD diagnostic criteria published in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition.

Prevalence and Characteristics of Autism Spectrum Disorder Among 4-Year-Old Children in the Autism and Developmental Disabilities Monitoring Network.

Objective: Early identification of children with autism spectrum disorder (ASD) facilitates timely access to intervention services. Yet, few population-based data exist on ASD identification among preschool-aged children. The authors aimed to describe ASD prevalence and characteristics among 4-year-old children in 5 of 11 sites participating in the 2010 Autism and Developmental Disabilities Monitoring Network. Method: Children with ASD were identified through screening of health and education records for ASD indicators, data abstraction and compilation for each child, and clinician review of records. ASD prevalence estimates, ages at first evaluation and ASD diagnosis, cognitive test scores, and demographics were compared for 4-year-old children and 8-year-old children living in the same areas. Results: Among 58,467 children in these 5 sites, 4-year-old ASD prevalence was 13.4 per 1000, which was 30% lower than 8-year-old ASD prevalence. Prevalence of ASD without cognitive impairment was 40% lower among 4-year-olds compared with 8-year-olds, but prevalence of ASD with cognitive impairment was 20% higher among 4-year-olds compared with 8-year-olds. Among 4-year-olds with ASD, female and non-Hispanic white children were more likely to receive their first comprehensive evaluation by age 36 months compared with male and non-Hispanic black children, respectively. Among children diagnosed with ASD by age 48 months, median age at first comprehensive evaluation was 27 months for 4-year-olds compared with 32 months for 8-year-olds. Conclusion: Population-based ASD surveillance among 4-year-old children provides valuable information about the early identification of children with ASD and suggests progression toward lowering the age of first ASD evaluation within participating Autism and Developmental Disabilities Monitoring communities.

On early sensitization to allergens and development of respiratory symptoms.

Various studies have suggested that a sequence of events occurring in childhood may affect the development of asthma in susceptible individuals. We have investigated whether early childhood sensitization to aeroallergens is an important risk factor in the later development of asthma symptoms.

Contribution of diet to aggregate arsenic exposures—An analysis across populations

The relative contribution of dietary arsenic (As) to aggregate daily exposure has not been well-characterized, especially in relation to the current EPA maximum contaminant level (MCL) of 10 p.p.b. for As in drinking water. Our objectives were to: (1) model exposure to inorganic and total As among non-seafood eaters using subject-specific data, (2) compare the contribution of food, drinking and cooking water to estimated aggregate exposure in households with variable background tap water As levels, and (3) describe the upper distribution of potential dose at different thresholds of tap water As. Dietary As intake was modeled in regional study populations and NHANES 2003–2004 using dietary records in conjunction with published food As residue data. Water As was measured in the regional studies. Among subjects exposed to tap water As >10 p.p.b., aggregate inorganic exposure was 24.5–26.1 μg/day, with approximately 30% of intake from food. Among subjects living in homes with tap water As ≤10, 5 or 3 p.p.b., aggregate inorganic As exposure was 8.6–11.8 μg/day, with 54–85% of intake from food. Median inorganic As potential dose was 0.42–0.50 μg/kg BW/day in subjects exposed to tap water As >10 p.p.b. and less than half that among subjects exposed to tap water As ≤10 p.p.b. The majority of inorganic and total As exposure is attributable to diet in subjects with tap water As <MCL. Further research is needed to determine the potential toxicity and need for regulation of As in foods.

The course of persistent airflow limitation in subjects with and without asthma

RATIONALE Most patients who develop persistent airflow limitation do so either as a manifestation of chronic obstructive pulmonary disease that is largely related to smoking or as a consequence of persistent asthma. We sought to compare the natural course of lung function associated with persistent airflow limitation in subjects with and without asthma from early to late adult life. METHODS We studied 2552 participants aged 25 or more who had multiple questionnaire and lung function data from the long-term prospective population-based Tucson Epidemiological Study of Airway Obstructive Disease. Persistent airflow limitation was defined as FEV(1)/FVC ratio consistently < 70% in all completed surveys subsequent to the first survey with airflow limitation. Participants were divided into nine groups based on the combination of their physician-confirmed asthma status (never, onset < or = 25 years, or onset > 25 years) and the presence of airflow limitation during the study follow-up (never, inconsistent, or persistent). RESULTS Among subjects with an asthma onset < or = 25 years, blood eosinophilia increased significantly the odds of developing persistent airflow limitation (adjusted ORs: 3.7, 1.4-9.5), whereas cigarette smoking was the strongest risk factor for persistent airflow limitation among non-asthmatics and among subjects with asthma onset after age 25 years. Among subjects with persistent airflow limitation, the natural course of lung function differed between subjects with asthma onset < or = 25 years and non-asthmatics, with the former having lower FEV(1) levels at age 25 (predicted value for a 175-cm tall male of 3400 versus 4090 ml, respectively; p<0.001) and the latter having greater FEV(1) loss between age 25 and 75 (1590 versus 2140 ml; p=0.003). CONCLUSION In subjects who have asthma onset before 25 years of age and persistent airflow limitation in adult life, the bulk of the FEV(1) deficit is already established before age 25 years.

Human exposure to dietary inorganic arsenic and other arsenic species: State of knowledge, gaps and uncertainties.

Inorganic arsenic (iAs) is ubiquitous in the environment as arsenite (AsIII) and arsenate (AsV) compounds and biotransformation of these toxic chemicals leads to the extraordinary variety of organoarsenic species found in nature. Despite classification as a human carcinogen based on data from populations exposed through contaminated drinking water, only recently has a need for regulatory limits on iAs in food been recognized. The delay was due to the difficulty in risk assessment of dietary iAs, which critically relies on speciation analysis providing occurrence data for iAs in food - and not simply for total arsenic. In the present review the state of knowledge regarding arsenic speciation in food and diet is evaluated with focus on iAs and human exposure assessment through different dietary approaches including duplicate diet studies, market basket surveys, and total diet studies. The analytical requirements for obtaining reliable data for iAs in food are discussed and iAs levels in foods and beverages are summarized, along with information on other (potentially) toxic co-occurring organoarsenic compounds. Quantitative exposure assessment of iAs in food is addressed, focusing on the need of capturing variability and extent of exposure and identifying what dietary items drive very high exposure for certain population groups. Finally, gaps and uncertainties are discussed, including effect of processing and cooking, and iAs bioavailability.

Acute cardiovascular effects of firefighting and active cooling during rehabilitation.

Objectives: To determine the cardiovascular and hemostatic effects of fire suppression and postexposure active cooling. Methods: Forty-four firefighters were evaluated before and after a 12-minute live-fire drill. Next, 50 firefighters performing the same drill were randomized to undergo postfire forearm immersion in 10°C water or standard rehabilitation. Results: In the first study, heart rate and core body temperature increased and serum C-reactive protein decreased but there were no significant changes in fibrinogen, sE-selectin, or sL-selectin. The second study demonstrated an increase in blood coagulability, leukocyte count, factors VIII and X, cortisol, and glucose, and a decrease in plasminogen and sP-selectin. Active cooling reduced mean core temperature, heart rate, and leukocyte count. Conclusions: Live-fire exposure increased core temperature, heart rate, coagulability, and leukocyte count; all except coagulability were reduced by active cooling.

Tracheobronchial Markers of Lung Injury in Smoke Inhalation Victims

Although smoke inhalation injury victims frequently develop severe hypoxemia and are at increased risk of acute respiratory distress syndrome (ARDS), no early prognostic tests are currently available. The objectives were to determine early longitudinal changes in tracheobronchial fluid inflammatory markers and assess the value of initial concentrations as predictors of subsequent lung injury. Partial pressure of arterial oxygen (Pao2) and the fraction of inspired oxygen (Fio2) were recorded approximately every 6 hours from intubated smoke inhalation victims admitted to a regional burn center. Tracheobronchial suction fluid was collected every 2 hours and assayed for interleukins (IL-1&bgr;, -8, and -10), tumor necrosis factor-&agr;, transforming growth factor-&bgr;1, soluble Fas ligand (sFasL), and complement factor 5a. Temporal trends in marker concentrations during 36 hours and the relations between initial concentrations and lowest Pao2/Fio2 or ARDS within 72 hours were assessed using random coefficients modeling and cross-sectional analysis. In 21 subjects with tracheobronchial samples collected within 6.5 hours of intubation, 14 (66.7%) developed acute hypoxemia (Pao2/Fio2 ≤200) within 72 hours of exposure and nine (42.9%) developed ARDS, as defined by the American-European consensus conference on ARDS. IL-8 increased sharply in the first 6.5 hours postexposure (P < .001), and IL-1&bgr; in the first 6.1 hours (P < .001). No significant temporal trends in IL-10, tumor necrosis factor-&agr;, transforming growth factor-&bgr;1, sFasL, or complement factor 5a were found. Only initial IL-8 was associated with increased Pao2/Fio2 (P = .013) and with a minimum Pao2/Fio2 >200 (P = .042) during 72 hours. In smoke inhalation victims, tracheobronchial IL-1&bgr; and IL-8 increase rapidly and high initial IL-8 may predict improved oxygenation.

Prenatal factors associated with the development of eczema in the first year of life.

Prenatal factors have been implicated in childhood eczema, but the relationship between maternal cytokine production during pregnancy and infant eczema is unknown. Non‐selected women in their third trimester were enrolled in the Tucson Infant Immune Study. Data from three sources were used to define MD‐eczema: parent‐completed illness questionnaires at age 2, 3, 4, 6 and 9 months regarding physician‐seen eczema, parent‐completed questionnaires at 12 months regarding physician‐diagnosed eczema, and medical record reviews. Blood samples were taken from mothers during their third trimester and from the umbilical cord at birth. Maternal peripheral blood mononuclear cells and cord blood mononuclear cells were stimulated with ConA/PMA, and supernatants were assayed for IFN‐γ and IL‐4, ‐5, ‐10, and ‐13. Of 364 children, 28% were seen by a physician for eczema by 1 yr of age. After adjustment for potential confounders using logistic regression, the odds for development of eczema in infancy were significantly higher when mothers had active eczema in pregnancy (OR, 2.46, CI 1.0–5.8, p < 0.042) and when mothers were in the highest tertile of serum IgE production (OR 2.28, CI 1.2–4.4, p < 0.013). Colds in the third trimester were associated with lower odds of eczema (OR 0.32, CI 0.16–0.63, p < 0.001). Our findings from this cohort study suggest that in utero factors, including maternal IgE, colds, and eczema, may influence the risk of infant eczema.

Measured versus modeled dietary arsenic and relation to urinary arsenic excretion and total exposure

Chronic exposure to arsenic (As) in food and water is a significant public health problem. Person-specific aggregate exposure is difficult to collect and modeling based on limited food As residue databases is of uncertain reliability. Two cross-sectional population exposure studies, the National Human Exposure Assessment Survey-Arizona and Arizona Border Survey, had a combined total of 252 subjects with diet, water, and urinary As data. Total As was measured in 24-h duplicate diet samples and modeled using 24-h diet diaries in conjunction with several published food surveys of As. Two-stage regression was used to assess the effects of dietary As on urinary total As (uAs): (1) generalized linear mixed models of uAs above versus below the limit of detection (LOD); and (2) restricted models limited to those subjects with uAs>LOD, using bootstrap sampling and mixed models adjusted for age, sex, body mass index, ethnicity, current smoking, and As intake from drinking and cooking water. In restricted models, measured and modeled estimates were significant predictors of uAs. Modeled dietary As based on Total Diet Study mean residues greatly underestimated the dietary intake. In households with tap water As ≤10 p.p.b., over 93% of total arsenic exposure was attributable to diet.