Validación de un Cuestionario para Evaluar Riesgo de Caries en Preescolares en Santiago, Chile / Validation of a Questionnaire to Assess Risk of Caries in Preschool-Age Children in Santiago, Chile

RESUMEN: La Caries Temprana de la Infancia (CTI) es una forma de caries dental agresiva que afecta a niños, y en el último reporte nacional reveló una prevalencia de caries del 50 % en niños de 4 años de edad de la Región Metropolitana de Santiago (Soto et al., 2007). El objetivo de este estudio es validar un cuestionario que permita recolectar información relacionada con diversos factores de riesgo de caries en niños preescolares. Para la validación del cuestionario se determinó la validez de convergencia y discriminación, la consistencia interna y la confiabilidad test retest del instrumento en dos muestras independientes. Se aplicó el instrumento al cuidador principal de 118 preescolares entre 24 a 71 meses de edad, que asisten a jardines infantiles de dependencia particular (bajo riesgo de caries) y la Fundación INTEGRA (alto riesgo de caries) en la Región Metropolitana de Santiago, Chile. Se realizaron exámenes clínicos dentales por 2 odontólogos calibrados utilizando en el criterio OMS e ICDAS II. Se estimó un modelo de regresión logística y se evalúo la capacidad de discriminación del puntaje a través de una curva ROC. El cuestionario mostró una validez de discriminación de 0,95 entre ambos grupos y de la pregunta global 0,61 y una consistencia interna del cuestionario de 0,72. En la validez de convergencia se encontró que no existe asociación estadísticamente significativa entre el puntaje del cuestionario y la pregunta global dicotomizada (OD) 1,061. No obstante, se evidenció que si existe asociación estadísticamente significativa entre el puntaje del cuestionario y el grupo riesgo de caries (bajo y alto) (OD) 1,961. La estabilidad temporal mediante comparaciones Test - Retest calculado con el índice de Kappa osciló entre 0,37 a 1. Por lo tanto, se puede concluir que el presente cuestionario es un instrumento válido para discriminar riesgo de caries, permitiendo un mejor análisis de los determinantes de la caries dental en la población preescolar chilena.

ABSTRACT: Early Childhood Caries (ECC) is an aggressive form of tooth decay, and the last national unpublished reports reveal a caries prevalence of 50 % at 4 years of age in children, in the Santiago Metropolitan Region (Soto et al., 2007). The objective of this study is to validate a questionnaire that allows the collection of information related to several caries risk factors in preschoolchildren. For the validation of the questionnaire, the convergence and discrimination validity, the internal consistency and the retest, test reliability of the instrument were determined in two independent samples. The instrument was applied to the main caregiver of 118 preschoolers between 24 and 71 months of age, who attend private childcare centers (low caries risk) and the INTEGRA Foundation childcare (high caries risk) in the Metropolitan Region of Santiago, Chile. Dental clinical examinations were performed by two calibrated dentists using the OMS and ICDAS II criteria. A logistic regression model was estimated and the ability to discriminate the score through an ROC curve was evaluated. The questionnaire showed a validity of discrimination of 0.95 between both groups and of the global question 0.61 and an internal consistency of the questionnaire of 0.72. In the convergence validity, it was found that there is no statistically significant association between the questionnaire score and the dichotomized global question (RE) 1.061. However, it was evidenced that there is a statistically significant association between the questionnaire score and the caries risk group (low and high) (OD) 1.961. Temporal stability by means of Test - Retest comparisons calculated with the Kappa index ranged from 0.37 to 1. Therefore, it can be concluded that the present questionnaire is a valid instrument for discriminating caries risk, allowing a better analysis of the determinants of dental caries in the Chilean preschool population.

The decrease in population bone lead levels in Canada between 1993 and 2010 as assessed by in vivo XRF.

Objective and Approach: A study, conducted in Toronto, Canada, between 2009 and 2011, measured the bone lead concentrations of volunteers aged 1-82 years using in vivo x-ray fluorescence (XRF) technology. MAIN RESULTS: Bone lead levels were lower compared to Ontario in vivo XRF studies from the early 1990s. In adults, the slope of tibia lead content versus age was reduced by 36-56%, i.e. bone lead levels for a given age group were approximately half compared to the same age group 17 years prior. Further, bone lead levels of individuals fell over that time period. In 2010, an average person aged 57 years had a bone lead level approximately 1/3 less than their bone lead level age 40 years in 1993. Using this data, the half-lives of lead in the tibia were estimated as 7-26 years. Tibia lead levels were found to be low in children. The reduction in bone tibia content in children was not significant (p = 0.07), but using data from additional north eastern US studies, there is evidence that childhood tibia stores are lower than in the 1990s. SIGNIFICANCE: In vivo XRF analysis shows that there has been a reduction in the level of lead in bone in Canada over the last two decades. Public health measures have been very successful in reducing ongoing exposure to lead and in reducing bone lead stores.

Age and sex influence on bone and blood lead concentrations in a cohort of the general population living in Toronto.

OBJECTIVE: To study the age and sex influence on bone and blood lead concentrations in a cohort of the general population living in Toronto. APPROACH: A 109Cd K x-ray fluorescence (KXRF) measurement system was used from 2009 to 2011 in a study that measured the bone lead (Pb) concentration of 263 environmentally exposed individuals residing in Toronto, Ontario, Canada. Tibia (cortical bone) and calcaneus (trabecular bone) lead contents were measured in 134 males and 129 females between 1 and 82 years of age. Whole blood Pb concentration was measured by TIMS (thermal ionization mass spectrometer). Tibia (Ti) and calcaneus (Cal) Pb were examined versus the age of participants, taking into account uncertainties in bone Pb measurement values. MAIN RESULTS: No significant sex differences were observed in any of the age categories. Participants older than 50 years of age demonstrated the highest concentrations of Pb in their blood, tibia, and calcaneus bones. SIGNIFICANCE: In most of the previous publications, uncertainty was not considered in the regression model of bone Pb and age. However, in this paper, we adjusted the bone Pb values for the uncertainty level. This had a significant influence in regression models of bone Pb and thus we recommend that uncertainty be considered in future studies.

Can changing the timing of outdoor air intake reduce indoor concentrations of traffic-related pollutants in schools?

Traffic emissions have been associated with a wide range of adverse health effects. Many schools are situated close to major roads, and as children spend much of their day in school, methods to reduce traffic-related air pollutant concentrations in the school environment are warranted. One promising method to reduce pollutant concentrations in schools is to alter the timing of the ventilation so that high ventilation time periods do not correspond to rush hour traffic. Health Canada, in collaboration with the Ottawa-Carleton District School Board, tested the effect of this action by collecting traffic-related air pollution data from four schools in Ottawa, Canada, during October and November 2013. A baseline and intervention period was assessed in each school. There were statistically significant (P < 0.05) reductions in concentrations of most of the pollutants measured at the two late-start (9 AM start) schools, after adjusting for outdoor concentrations and the absolute indoor-outdoor temperature difference. The intervention at the early-start (8 AM start) schools did not have significant reductions in pollutant concentrations. Based on these findings, changing the timing of the ventilation may be a cost-effective mechanism of reducing traffic-related pollutants in late-start schools located near major roads.

Validation of QuickScan dicentric chromosome analysis for high throughput radiation biological dosimetry.

Currently, the dicentric chromosome assay (DCA) is used to estimate radiation doses to individuals following accidental radiological and nuclear overexposures when traditional dosimetry methods are not available. While being an exceptionally sensitive method for estimating doses by radiation, conventional DCA is time-intensive and requires highly trained expertise for analysis. For this reason, in a mass casualty situation, triage-quality conventional DCA struggles to provide dose estimations in a timely manner for triage purposes. In Canada, a new scoring technique, termed DCA QuickScan, has been devised to increase the throughput of this assay. DCA QuickScan uses traditional DCA sample preparation methods while adapting a rapid scoring approach. In this study, both conventional and QuickScan methods of scoring the DCA assay were compared for accuracy and sensitivity. Dose response curves were completed on four different donors based on the analysis of 1,000 metaphases or 200 events at eight to nine dose points by eight different scorers across two laboratories. Statistical analysis was performed on the data to compare the two methods within and across the laboratories and to test their respective sensitivities for dose estimation. This study demonstrated that QuickScan is statistically similar to conventional DCA analysis and is capable of producing dose estimates as low as 0.1 Gy but up to six times faster. Therefore, DCA QuickScan analysis can be used as a sensitive and accurate method for scoring samples for radiological biodosimetry in mass casualty situations or where faster dose assessment is required.

Evaluating the biological effects of intermittent 1.9 GHz pulse-modulated radiofrequency fields in a series of human-derived cell lines.

Several recent studies have suggested that radiofrequency (RF) fields may cause changes in a variety of cellular functions that may eventually lead to potential long-term health effects. In the present study, we have assessed the ability of non-thermal RF-field exposure to affect a variety of biological processes (including apoptosis, cell cycle progression, viability and cytokine production) in a series of human-derived cell lines (TK6, HL60 and Mono-Mac-6). Exponentially growing cells were exposed to intermittent (5 min on, 10 min off) 1.9 GHz pulse-modulated RF fields for 6 h at mean specific absorption rates (SARs) of 0, 1 and 10 W/kg. Concurrent negative (incubator) and positive (heat shock for 1 h at 43 degrees C) controls were included in each experiment. Immediately after the 6-h exposure period and 18 h after exposure, cell pellets were collected and analyzed for cell viability, the incidence of apoptosis, and alterations in cell cycle kinetics. The cell culture supernatants were assessed for the presence of a series of human inflammatory cytokines (TNFA, IL1B, IL6, IL8, IL10, IL12) using a cytometric bead array assay. No detectable changes in cell viability, cell cycle kinetics, incidence of apoptosis, or cytokine expression were observed in any of RF-field-exposed groups in any of the cell lines tested, relative to the sham controls. However, the positive (heat-shock) control samples displayed a significant decrease in cell viability, increase in apoptosis, and alteration in cell cycle kinetics (G(2)/M block). Overall, we found no evidence that non-thermal RF-field exposure could elicit any detectable biological effect in three human-derived cell lines.

Exposure to chronic noise and fractionated X-ray radiation elicits biochemical changes and disrupts body weight gain in rat.

The aim was to assess the developmental and biochemical effects resulting from separate and combined exposures to radiation and noise in adult male Sprague-Dawley rats. For 21 days, animals were exposed daily (1) to whole-body 121 kVp X-ray exposure (cumulative dose=5 Gy), (2) to random intermittent noise band-limited between 0.4 and 20 kHz; 2 h day(-1) 86 decibels (dB) and (3) to combined exposures. Control animals were housed under ambient noise conditions 55 dB A-weighted (dBA) and sham-exposed to X-rays. Body weight gain was significantly reduced in animals exposed to either X-rays or noise, and the loss was more pronounced in animals exposed to both conditions. Neither plasma adrenocorticotropic hormone (ACTH) nor corticosterone was altered by the treatment conditions. This study corroborated previous reports that ionizing radiation exposure increased plasma levels of 8-hydroxy-2'-deoxyguanosine (8-OHDG), but no effect was observed in animals co-exposed to chronic noise. Plasma big-endothelin-1 (Big ET-1) was significantly reduced in animals exposed to a combination of noise and X-rays. The results indicated that (1) adaptation to chronic noise appeared to occur at the level of the hypothalamic pituitary adrenal (HPA) response, in spite of a compromise in overall body weight gain; and (2) ionizing radiation exposure might alter systems activated by stressor exposure and/or act independently to influence health outcomes.

Effects of postnatal exposure to mixtures of non-ortho-PCBs, PCDDs, and PCDFs in prepubertal female rats.

There are concerns that postnatal exposure to organochlorines present in breast milk could lead to adverse health effects. We reconstituted four mixtures of aryl-hydrocarbon receptor (AhR) agonists (3 non-ortho polychlorinated biphenyls [PCBs], 6 polychlorinated dibenzodioxins [PCDDs], 7 polychlorinated dibenzofurans [PCDFs], or all 16 chemicals together [referred to as AhRM]) based on their concentrations in breast milk, and examined their effects following exposure by gavage from day 1 until day 20 of age. Female neonates received dosages of AhRM equivalent to 1, 10, 100, or 1000 times the amount consumed by an infant over the first 24 days of life. Other groups received the PCBs, the PCDDs, or the PCDFs at the 1000x level. All rats were sacrificed at 21 days of age. Changes in ethoxyresorufin-o-deethylase hepatic activity, thymus and body weights, and serum thyroxin were linked to the 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxic equivalents (TEQ) of the four mixtures (1000x-AhRM > PCDDs > PCBs > PCDFs). To test for AhRM antiestrogenicity, two additional groups received 1.5 microg/kg of 17alpha-ethynyl estradiol (EE) with or without the 1000x-AhRM. The AhRM had no effect on uterine weight or EE-stimulated uterine growth. The actions of the combined EE and AhRM treatments suggest additive effects in decreasing pentoxyresorufin-o-deethylase activity and spleen weight, but nonadditive/antagonistic effects on adrenal weight and serum thyroxin. In conclusion, (1) 10x-AhRM had no detectable effects, (2) TEQ values relate to observed toxicities, even when testing complex mixtures of AhR agonists, and (3) indications of tissue-specific additive and nonadditive/antagonistic effects, but no synergism, were observed when doses of AhRM were increased, or combined with EE.

No evidence for genotoxic effects from 24 h exposure of human leukocytes to 1.9 GHz radiofrequency fields.

The current study extends our previous investigations of 2-h radiofrequency (RF)-field exposures on genotoxicity in human blood cell cultures by examining the effect of 24-h continuous-wave (CW) and pulsed-wave (PW) 1.9 GHz RF-field exposures on both primary DNA damage and micronucleus induction in human leukocyte cultures. Mean specific absorption rates (SARs) ranged from 0 to 10 W/kg, and the temperature within the cultures was maintained at 37.0 +/- 1.0 degrees C for the duration of the 24-h exposure period. No significant differences in primary DNA damage were observed between the sham-treated controls and any of the CW or PW 1.9 GHz RF-field-exposed cultures when processed immediately after the exposure period by the alkaline comet assay. Similarly, no significant differences were observed in the incidence of micronuclei, incidence of micronucleated binucleated cells, frequency of binucleated cells, or proliferation index between the sham-treated controls and any of the CW or PW 1.9 GHz RF-field-exposed cultures. In conclusion, the current study found no evidence of 1.9 GHz RF-field-induced genotoxicity in human blood cell cultures after a 24-h exposure period.

DNA damage and micronucleus induction in human leukocytes after acute in vitro exposure to a 1.9 GHz continuous-wave radiofrequency field.

Human blood cultures were exposed to a 1.9 GHz continuous-wave (CW) radiofrequency (RF) field for 2 h using a series of six circularly polarized, cylindrical waveguides. Mean specific absorption rates (SARs) of 0.0, 0.1, 0.26, 0.92, 2.4 and 10 W/kg were achieved, and the temperature within the cultures during a 2-h exposure was maintained at 37.0 +/- 0.5 degrees C. Concurrent negative (incubator) and positive (1.5 Gy (137)Cs gamma radiation) control cultures were run for each experiment. DNA damage was quantified immediately after RF-field exposure using the alkaline comet assay, and four parameters (tail ratio, tail moment, comet length and tail length) were used to assess DNA damage for each comet. No evidence of increased primary DNA damage was detected by any parameter for RF-field-exposed cultures at any SAR tested. The formation of micronuclei in the RF-field-exposed blood cell cultures was assessed using the cytokinesis-block micronucleus assay. There was no significant difference in the binucleated cell frequency, incidence of micronucleated binucleated cells, or total incidence of micronuclei between any of the RF-field-exposed cultures and the sham-exposed controls at any SAR tested. These results do not support the hypothesis that acute, nonthermalizing 1.9 GHz CW RF-field exposure causes DNA damage in cultured human leukocytes.

DNA damage in human leukocytes after acute in vitro exposure to a 1.9 GHz pulse-modulated radiofrequency field.

Blood cultures from human volunteers were exposed to an acute 1.9 GHz pulse-modulated radiofrequency (RF) field for 2 h using a series of six circularly polarized, cylindrical waveguides. Mean specific absorption rates (SARs) ranged from 0 to 10 W/kg, and the temperature within the cultures during the exposure was maintained at 37.0 +/- 0.5 degrees C. DNA damage was quantified in leukocytes by the alkaline comet assay and the cytokinesis-block micronucleus assay. When compared to the sham-treated controls, no evidence of increased primary DNA damage was detected by any parameter for any of the RF-field-exposed cultures when evaluated using the alkaline comet assay. Furthermore, no significant differences in the frequency of binucleated cells, incidence of micronucleated binucleated cells, or total incidence of micronuclei were detected between any of the RF-field-exposed cultures and the sham-treated control at any SAR tested. These results do not support the hypothesis that acute, nonthermalizing 1.9 GHz pulse-modulated RF-field exposure causes DNA damage in cultured human leukocytes.

DNA damage and apoptosis in the immature mouse cerebellum after acute exposure to a 1 mT, 60 Hz magnetic field.

Several recent studies have reported that whole-body exposure of rodents to power frequency magnetic fields (MFs) can result in DNA single- and double-strand breaks in the brains of these animals. The current study was undertaken to investigate whether an acute 2h exposure of a 1 mT, 60 Hz MF could elicit DNA damage, and subsequently apoptosis, in the brains of immature (10-day-old) mice. DNA damage was quantitated at 0, 2, 4, and 24h after exposure using the alkaline comet assay. Apoptosis was quantitated in the external granule cell layer (EGCL) of the immature mouse cerebellum at 0 and 24h after exposure to MF by the TdT-mediated dUTP nick-end labeling (TUNEL) assay. Four parameters (tail ratio, tail moment, comet length and tail length) were used to assess DNA damage for each comet. While increased DNA damage was detected by tail ratio at 2h after MF exposure, no supporting evidence of increased DNA damage was detected by the other parameters. In addition, no similar differences were observed using these parameters at any of the other post-exposure times. No increase in apoptosis was observed in the EGCL of MF-exposed mice, when compared to sham mice. Taken together, these results do not support the hypothesis that acute MF exposure causes DNA damage in the cerebellums of immature mice.

A comparison of methods for estimating the benchmark dose based on overdispersed data from developmental toxicity studies.

Developmental anomalies resulting from prenatal toxicity can be manifested in terms of both malformations among surviving offspring and prenatal death. Although these two endpoints have traditionally been analyzed separately in the assessment of risk, multivariate methods of risk characterization have recently been proposed. We examined this and other issues in developmental toxicity risk assessment by evaluating the accuracy and precision of estimates of the effective dose (ED05) and the benchmark dose (BMD05) using computer simulation. Our results indicated that different variance structures (Dirichlet-trinomial and generalized linear model) used to characterize overdispersion yielded comparable results when fitting joint dose response models based on generalized estimating equations. (The choice of variance structure in separate modeling was also not critical.) However, using the Rao-Scott transformation to eliminate overdispersion tended to produce estimates of the ED05 with reduced bias and mean squared error. Because joint modeling ensures that the ED05 for overall toxicity (based on both malformations and prenatal death) is always less than the ED05 for either malformations or prenatal death, joint modeling is preferred to separate modeling for risk assessment purposes.