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We compared the prevalence of various medical and behavioral co-occurring conditions/symptoms between 4- and 8-year-olds with autism spectrum disorder (ASD) from five sites in the Autism and Developmental Disabilities Monitoring Network during the 2010 survey year, accounting for sociodemographic differences. Over 95% of children had at least one co-occurring condition/symptom. Overall, the prevalence was higher in 8- than 4-year-olds for 67% of co-occurring conditions/symptoms examined. Further, our data suggested that co-occurring conditions/symptoms increased or decreased the age at which children were first evaluated for ASD. Similarly, among the 8-year-olds, the prevalence of most co-occurring conditions/symptoms was higher in children with a previous ASD diagnosis documented in their records. These findings are informative for understanding and screening co-occurring conditions/symptoms in ASD.

We compared early-diagnosed autism spectrum disorder (ASD) (defined as diagnosis by age 4 years) between the 2002 and 2006 birth cohorts, in five sites of the Autism and Developmental Disabilities Monitoring Network. In the 2002 cohort, the prevalence/1000 of early-diagnosed ASD was half the 8-year-old prevalence (7.2 vs. 14.7, prevalence ratio [PR] 0.5 [0.4–0.6]). Overall, the prevalence of early-diagnosed ASD did not differ between birth cohorts (PR 1.1 [0.9–1.3]). However, in three sites with complete case ascertainment, the prevalence of early-diagnosed ASD was higher for those born in 2006 versus 2002 (PR 1.3 [1.1–1.5]), suggesting possible improvement in early identification. The lack of change in two sites may reflect less complete case ascertainment. Studies in more recent cohorts are needed.

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.

Objective: Heart disease is the leading cause of firefighter line-of-duty deaths. The study objectives were to identify early atherosclerotic disease through ultrasound measurement of carotid intima-media thickness (CIMT) and risk factors predicting increased CIMT and carotid plaque. Methods: Following ultrasound evaluation of 597 Phoenix and Tucson firefighters, logistic regression was used to identify risk factors for mean CIMT greater than 75th percentile and for carotid plaque. Results: Age, low-density lipoprotein cholesterol (LDL-C) of 100 mg/dL or more, and high-density lipoprotein cholesterol were significant independent predictors of increased CIMT. Age, hypertension, LDL-C, and plasma soluble P-selectin were significant predictors of carotid plaque. Conclusions: This study supports an emphasis on traditional risk factors for atherosclerotic disease in firefighters, in particular maintaining LDL-C less than 100 mg/dL. Plasma soluble P-selectin may help identify firefighters at increased risk for carotid plaque.

Objective: To investigate whether genetic vanants involved in cytokine expression are associated with the age-related rate of decline in forced expiratory volume in 1 second (FEV₁). Methods: Functional polymorphisms in the TNFα, TGFβ₁, IL-1β, IL-1RN, IL-13, and IL-8 genes were investigated in 374 active firefighters with at least five pulmonary function tests. Results: A protective effect was found between the presence of the TGFβ1 -509 TT genotype and rate of decline in FEV₁ (P = 0.043). Carrying an A allele at TNFα -308 (P = 0.010) and GG genotype at TNFβ -238 (P = 0.028) was associated with a more rapid rate of FEV₁ decline. The TNFα -308A/-238G haplotype was also associated with an increased rate of decline as compared with the other haplotypes. Conclusions: Interindividual vanability in progressive decline in FEV₁ may be explained in part by genetic variations within genes involved in inflammatory responses.

Objective: We conducted this study to evaluate the association of cytokine genotypes and sputum concentrations on longitudinal decline in lung function in firefighters. Methods: In 67 firefighters with at least four pulmonary function tests, DNA was analyzed for functional polymorphisms of interleukin (IL)-1β, IL-1 receptor antagonist (IL1RA), IL-8, IL-10, tumor necrosis factor-alpha (TNF-α) genes, and sputum evaluated for cytokine concentration by ELISA. Results: The annual rate of FEV1 decline was greater in firefighters with TT genotypes at IL-10 (-819) (P = 0.009) and with CT or TT genotypes at IL-1RA (2018) (P = 0.050). These genotypes were not associated with concentrations of sputum cytokine, but increased IL-1RA was associated with a slower rate of FEV1 decline (P = 0.025), as was increased sputum macrophage count (P = 0.002). Conclusions: Cytokine genotypes were associated with the rate of FEV1 decline but did not alter concentrations of sputum cytokine. Increased sputum IL-1RA may be protective.

The study was conducted to measure the effectiveness of providing bottled water in reducing arsenic exposure. Urine, tap-water and toenail samples were collected from non-smoking adults residing in Ajo (n=40) and Tucson (n=33), Arizona, USA. The Ajo subjects were provided bottled water for 12 months prior to re-sampling. The mean total arsenic (μg/L) in tap-water was 20.3±3.7 in Ajo and 4.0±2.3 in Tucson. Baseline urinary total inorganic arsenic (μg/L) was significantly higher among the Ajo subjects (n=40, 29.1±20.4) than among the Tucson subjects (n=32, 11.0±12.0, p<0.001), as was creatinine-adjusted urinary total inorganic arsenic (μg/g) (35.5±25.2 vs 13.2±9.3, p<0.001). Baseline concentrations of arsenic (μg/g) in toenails were also higher among the Ajo subjects (0.51±0.72) than among the Tucson subjects (0.17±0.21) (p<0.001). After the intervention, the mean urinary total inorganic arsenic in Ajo (n=36) dropped by 21%, from 29.4±21.1 to 23.2±23.2 (p=0.026). The creatinine-adjusted urinary total inorganic arsenic and toenail arsenic levels did not differ significantly with the intervention. Provision of arsenic-free bottled water resulted in a modest reduction in urinary total inorganic arsenic.

The diagnosis of autism spectrum disorder (ASD) is often delayed from the time of noted concerns to the actual diagnosis. The current study used child- and family-level factors to identify homogeneous classes in a surveillance-based sample (n = 2303) of 8-year-old children with ASD. Using latent class analysis, a 5-class model emerged and the class memberships were examined in relation to the child’s median age at ASD diagnosis. Class 3, with known language delays and a high advantage socioeconomically had the lowest age of ASD diagnosis (46.74 months) in comparison to Classes 1 (64.99 months), 4 (58.14 months), and 5 (69.78 months) in this sample. Findings demonstrate sociodemographic and developmental disparities related to the age at ASD diagnosis.

The diet is emerging as the dominant source of arsenic exposure for most of the U.S. population. Despite this, limited regulatory efforts have been aimed at mitigating exposure, and the role of diet in arsenic exposure and disease processes remains understudied. In this brief, we discuss the evidence linking dietary arsenic intake to human disease and discuss challenges associated with exposure characterization and efforts to quantify risks. In light of these challenges, and in recognition of the potential longer-term process of establishing regulation, we introduce a framework for shorter-term interventions that employs a field-to-plate food supply chain model to identify monitoring, intervention, and communication opportunities as part of a multisector, multiagency, science-informed, public health systems approach to mitigation of dietary arsenic exposure. Such an approach is dependent on coordination across commodity producers, the food industry, nongovernmental organizations, health professionals, researchers, and the regulatory community. https://doi.org/10.1289/EHP3997.

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  μ g/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  μ g/day, with 54–85% of intake from food. Median inorganic As potential dose was 0.42–0.50  μ g/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

Journal Article

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