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1.
BackgroundNumerous cross-sectional studies of school-age children have observed that exposure to manganese (Mn) adversely affects neurodevelopment. However, few prospective studies have looked at the effects of both prenatal and postnatal Mn exposure on child neurodevelopment.MethodsWe measured Mn levels in prenatal and early postnatal dentine of shed teeth and examined their association with behavior, cognition, memory, and motor functioning in 248 children aged 7, 9, and/or 10.5 years living near agricultural fields treated with Mn-containing fungicides in California. We used generalized linear models and generalized additive models to test for linear and nonlinear associations, and generalized estimating equation models to assess longitudinal effects.ResultsWe observed that higher prenatal and early postnatal Mn levels in dentine of deciduous teeth were adversely associated with behavioral outcomes, namely internalizing, externalizing, and hyperactivity problems, in boys and girls at 7 and 10.5 years. In contrast, higher Mn levels in prenatal and postnatal dentine were associated with better memory abilities at ages 9 and 10.5, and better cognitive and motor outcomes at ages 7 and 10.5 years, among boys only. Higher prenatal dentine Mn levels were also associated with poorer visuospatial memory outcomes at 9 years and worse cognitive scores at 7 and 10.5 years in children with higher prenatal lead levels (≥ 0.8 μg/dL). All these associations were linear and were consistent with findings from longitudinal analyses.ConclusionsWe observed that higher prenatal and early postnatal Mn levels measured in dentine of deciduous teeth, a novel biomarker that provides reliable information on the developmental timing of exposures to Mn, were associated with poorer behavioral outcomes in school-age boys and girls and better motor function, memory, and/or cognitive abilities in school-age boys. Additional research is needed to understand the inconsistencies in the neurodevelopmental findings across studies and the degree to which differences may be associated with different Mn exposure pathways and biomarkers.  相似文献   

2.
BackgroundBrain growth and structural organization occurs in stages beginning prenatally. Toxicants may impact neurodevelopment differently dependent upon exposure timing and fetal sex.ObjectivesWe implemented innovative methodology to identify sensitive windows for the associations between prenatal particulate matter with diameter  2.5 μm (PM2.5) and children's neurodevelopment.MethodsWe assessed 267 full-term urban children's prenatal daily PM2.5 exposure using a validated satellite-based spatio-temporally resolved prediction model. Outcomes included IQ (WISC-IV), attention (omission errors [OEs], commission errors [CEs], hit reaction time [HRT], and HRT standard error [HRT-SE] on the Conners' CPT-II), and memory (general memory [GM] index and its components — verbal [VEM] and visual [VIM] memory, and attention-concentration [AC] indices on the WRAML-2) assessed at age 6.5 ± 0.98 years. To identify the role of exposure timing, we used distributed lag models to examine associations between weekly prenatal PM2.5 exposure and neurodevelopment. Sex-specific associations were also examined.ResultsMothers were primarily minorities (60% Hispanic, 25% black); 69% had ≤ 12 years of education. Adjusting for maternal age, education, race, and smoking, we found associations between higher PM2.5 levels at 31–38 weeks with lower IQ, at 20–26 weeks gestation with increased OEs, at 32–36 weeks with slower HRT, and at 22–40 weeks with increased HRT-SE among boys, while significant associations were found in memory domains in girls (higher PM2.5 exposure at 18–26 weeks with reduced VIM, at 12–20 weeks with reduced GM).ConclusionsIncreased PM2.5 exposure in specific prenatal windows may be associated with poorer function across memory and attention domains with variable associations based on sex. Refined determination of time window- and sex-specific associations may enhance insight into underlying mechanisms and identification of vulnerable subgroups.  相似文献   

3.
BackgroundWhereas it is well established that prenatal exposure to polychlorinated biphenyls (PCBs) can disrupt children's behavior, early postnatal exposure has received relatively little attention in environmental epidemiology.ObjectivesTo evaluate prenatal and postnatal exposures to PCB-153, a proxy of total PCB exposure, and their relation to inattention and activity in 5-year-old Inuits from the Cord Blood Monitoring Program.MethodsPrenatal exposure to PCBs was informed by cord plasma PCB-153 levels. We used a validated pharmacokinetic model to estimate monthly infants' levels across the first year of life. Inattention and activity were assessed by coding of video recordings of children undergoing fine motor testing. We used multivariable linear regression to evaluate the association between prenatal and postnatal PCB-153 levels and inattention (n = 97) and activity (n = 98) at 5 years of age.ResultsCord plasma PCB-153 was not associated with inattention and activity. Each interquartile range (IQR) increase in estimated infant PCB-153 levels at 2 months was associated with a 1.02% increase in the duration of inattention (95% CI: 0.04, 2.00). Statistical adjustment for the duration of breastfeeding slightly increased regression coefficients for postnatal level estimates, some of which became statistically significant for inattention (months: 2–4) and activity (months: 2–5).ConclusionsOur study adds to the growing evidence of postnatal windows of development during which children are more susceptible to neurotoxicants like PCBs.  相似文献   

4.
Concerns over adverse effects of air pollution on children's health have been rapidly rising. However, the effects of air pollution on childhood growth remain to be poorly studied. We investigated the association between prenatal and postnatal exposure to PM10 and children's weight from birth to 60 months of age. This birth cohort study evaluated 1129 mother-child pairs in South Korea. Children's weight was measured at birth and at six, 12, 24, 36, and 60 months. The average levels of children's exposure to particulate matter up to 10 μm in diameter (PM10) were estimated during pregnancy and during the period between each visit until 60 months of age. Exposure to PM10 during pregnancy lowered children's weight at 12 months. PM10 exposure from seven to 12 months negatively affected weight at 12, 36, and 60 months. Repeated measures of PM10 and weight from 12 to 60 months revealed a negative association between postnatal exposure to PM10 and children's weight. Children continuously exposed to a high level of PM10 (> 50 μg/m3) from pregnancy to 24 months of age had weight z-scores of 60 that were 0.44 times lower than in children constantly exposed to a lower level of PM10 (≤ 50 μg/m3) for the same period. Furthermore, growth was more vulnerable to PM10 exposure in children with birth weight < 3.3 kg than in children with birth weight > 3.3 kg. Air pollution may delay growth in early childhood and exposure to air pollution may be more harmful to children when their birth weight is low.  相似文献   

5.
Pyrethroid insecticides are widely used in agriculture and in homes. Despite the neurotoxicity of these insecticides at high doses, few studies have examined whether lower-level exposures could adversely affect children's neurodevelopment.The PELAGIE cohort included 3421 pregnant women from Brittany, France between 2002 and 2006. When their children reached their sixth birthday, 428 mothers from the cohort were randomly selected, successfully contacted and found eligible. A total of 287 (67%) mothers agreed to participate with their children in the neuropsychological follow-up. Two cognitive domains were assessed by the Wechsler Intelligence Scale for Children: verbal comprehension and working memory. Five pyrethroid and two organophosphate insecticide metabolites were measured in maternal and child first-void urine samples collected between 6 and 19 gestational weeks and at 6 years of age, respectively. Linear regression models were used to estimate associations between cognitive scores and urinary pyrethroid metabolite concentrations, adjusting for organophosphate metabolite concentrations and potential confounders.Maternal prenatal pyrethroid metabolite concentrations were not consistently associated with any children's cognitive scores. By contrast, childhood 3-PBA and cis-DBCA concentrations were both negatively associated with verbal comprehension scores (P-trend = 0.04 and P-trend < 0.01, respectively) and with working memory scores (P-trend = 0.05 and P-trend < 0.01, respectively). No associations were observed for the three other childhood pyrethroid metabolite concentrations (4-F-3-PBA, cis-DCCA, and trans-DCCA).Low-level childhood exposures to deltamethrin (as cis-DBCA is its principal and selective metabolite), in particular, and to pyrethroid insecticides, in general (as reflected in levels of the 3-PBA metabolite) may negatively affect neurocognitive development by 6 years of age. Whatever their etiology, these cognitive deficits may be of importance educationally, because cognitive impairments in children interfere with learning and social development. Potential causes that can be prevented are of paramount public health importance.  相似文献   

6.
BackgroundPrenatal exposure to environmental levels of organochlorines (OCs) has been demonstrated to have immunotoxic effects in humans. We investigated the relationship between prenatal exposure to OCs and the occurrence of otitis media (OM) among Inuit children in Greenland.MethodsWe estimated the concentration of 14 PCB congeners and 11 pesticides in maternal and cord blood samples and in breast milk in a population-based cohort of 400 mother–child pairs. At follow-up, we examined the children's ears and used their medical records to assess the OM occurrence and severity. Multivariate regression analyses were used with adjustments for passive smoking, crowding, dietary habits, parent's educational level, breast feeding and the use of child-care.ResultsThe children were 4–10 years of age at follow-up and 223 (85%) participated. We found no association between prenatal OC exposure and the development of OM. Factors associated with the child's hazard of OM during the first 4 years of life were: mother's history of OM (HR 1.70, 95% CI 1.11–2.59, p = 0.01); mother's smoking habits: current (HR 2.47, 95% CI 1.45–4.21, p < 0.01) and previous (HR 2.00, 95% CI 1.19–3.36, p < 0.01); number of smokers in the home (HR 1.17, 95% CI 1.05–1.31, p < 0.01). After adjustment mothers' smoking habits remained significant.ConclusionWe found no relationship between high levels of prenatal exposure of OCs and occurrence of OM. Passive smoking was found as the strongest environmental risk factor for the development of OM.Interventions to reduce passive smoke in children's environment are needed.  相似文献   

7.
BackgroundPesticides are associated with poorer neurodevelopmental outcomes, but little is known about the effects on sensory functioning.MethodsAuditory brainstem response (ABR) and pesticide data were available for 27 healthy, full-term 9-month-old infants participating in a larger study of early iron deficiency and neurodevelopment. Cord blood was analyzed by gas chromatography–mass spectrometry for levels of 20 common pesticides. The ABR forward-masking condition consisted of a click stimulus (masker) delivered via ear canal transducers followed by an identical stimulus delayed by 8, 16, or 64 milliseconds (ms). ABR peak latencies were evaluated as a function of masker-stimulus time interval. Shorter wave latencies reflect faster neural conduction, more mature auditory pathways, and greater degree of myelination. Linear regression models were used to evaluate associations between total number of pesticides detected and ABR outcomes. We considered an additive or synergistic effect of poor iron status by stratifying our analysis by newborn ferritin (based on median split).ResultsInfants in the sample were highly exposed to pesticides; a mean of 4.1 pesticides were detected (range 0–9). ABR Wave V latency and central conduction time (CCT) were associated with the number of pesticides detected in cord blood for the 64 ms and non-masker conditions. A similar pattern seen for CCT from the 8 ms and 16 ms conditions, although statistical significance was not reached. Increased pesticide exposure was associated with longer latency. The relation between number of pesticides detected in cord blood and CCT depended on the infant's cord blood ferritin level. Specifically, the relation was present in the lower cord blood ferritin group but not the higher cord blood ferritin group.ConclusionsABR processing was slower in infants with greater prenatal pesticide exposure, indicating impaired neuromaturation. Infants with lower cord blood ferritin appeared to be more sensitive to the effects of prenatal pesticide exposure on ABR latency delay, suggesting an additive or multiplicative effect.  相似文献   

8.
BackgroundPrenatal exposure to air pollutants has recently been identified as a potential risk factor for neuropsychological impairment.ObjectivesTo assess whether prenatal exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2) and benzene were associated with impaired development in infants during their second year of life.MethodsRegression analyses, based on 438 mother–child pairs, were performed to estimate the association between mother exposure to air pollutants during pregnancy and neurodevelopment of the child. The average exposure to PM2.5, NO2 and benzene over the whole pregnancy was calculated for each woman. During the second year of life, infant neuropsychological development was assessed using the Bayley Scales of Infant Development. Regression analyses were performed to estimate the association between exposure and outcomes, accounting for potential confounders.ResultsWe estimated that a 1 μg/m3 increase during pregnancy in the average levels of PM2.5 was associated with a − 1.14 point decrease in motor score (90% CI: − 1.75; − 0.53) and that a 1 μg/m3 increase of NO2 exposure was associated with a − 0.29 point decrease in mental score (90% CI: − 0.47; − 0.11). Benzene did not show any significant association with development. Considering women living closer (≤ 100 m) to metal processing activities, we found that motor scores decreased by − 3.20 (90% CI: − 5.18; − 1.21) for PM2.5 and − 0.51 (− 0.89; − 0.13) for NO2, while mental score decreased by − 2.71 (90% CI: − 4.69; − 0.74) for PM2.5, and − 0.41 (9% CI: − 0.76; − 0.06) for NO2.ConclusionsOur findings suggest that prenatal residential exposure to PM2.5 and NO2 adversely affects infant motor and cognitive developments. This negative effect could be higher in the proximity of metal processing plants.  相似文献   

9.
BackgroundPolychlorinated dibenzo-p-dioxins/dibenzofurans (dioxins) and polychlorinated biphenyls (PCBs) are persistent organic pollutants (POPs) with potentially adverse impact on child neurodevelopment. Whether the potential detrimental effects of dioxins and PCBs on neurodevelopment are of specific or unspecific character is not clear.ObjectivesThe purpose of the current study was to examine the influence of maternal dietary exposure to dioxins and PCBs on ADHD symptoms and cognitive functioning in preschoolers. We aimed to investigate a range of functions, in particular IQ, expressive language, and executive functions.Material and methodsThis study includes n = 1024 children enrolled in a longitudinal prospective study of ADHD (the ADHD Study), with participants recruited from The Norwegian Mother and Child Cohort Study (MoBa). Boys and girls aged 3.5 years participated in extensive clinical assessments using well-validated tools; The Preschool Age Psychiatric Assessment interview (PAPA), Stanford-Binet 5th revision (SB-5), Child Development Inventory (CDI), and Behavior Rating Inventory of Executive Function, Preschool version (BRIEF-P). Maternal dietary exposure to dioxins and PCBs was estimated based on a validated food frequency questionnaire (FFQ) answered mid-pregnancy and a database of dioxin and PCB concentrations in Norwegian foods. Exposure to dioxins and dioxin-like PCBs (dl-compounds) was expressed in total toxic equivalents (TEQ), and PCB-153 was used as marker for non-dioxin-like PCBs (ndl-PCBs). Generalized linear and additive models adjusted for confounders were used to examine exposure-outcome associations.ResultsExposure to PCB-153 or dl-compound was not significantly associated with any of the outcome measures when analyses were performed for boys and girls together. After stratifying by sex, adjusted analyses indicated a small inverse association with language in girls. An increase in the exposure variables of 1 SD was associated with a reduction in language score of − 0.2 [CI − 0.4, − 0.1] for PCB-153 and − 0.2 [CI − 0.5, − 0.1] for dl-compounds in girls. For boys, exposure to PCB-153 or dl-compounds was not associated with language skills. The difference between sex-specific associations was not statistically significant (p-value = 0.13). No sex-specific effects were observed for ADHD-symptoms, IQ scores, or executive functions.ConclusionsWe found no indications that variation in current low-level exposure to PCB-153 or dl-compounds in Norway is associated with variation ADHD-symptoms, verbal/non-verbal IQ, or executive functions including working memory in preschoolers. However, our findings indicated that maternal dietary exposure to PCB-153 or dl-compounds during pregnancy was significantly associated with poorer expressive language skills in preschool girls, although the sex-specific associations were not significantly different.  相似文献   

10.
BackgroundInfants are exposed to persistent environmental contaminants through breast milk, yet studies assessing the health effects of postnatal exposure are lacking. Existing postnatal exposure assessment is either too simple (lactation exposure model, LEM) or requires complex physiologically-based pharmacokinetic (PBPK) models.ObjectivesWe present equations for postnatal exposure calculations. We applied these equations to study the effect of hexachlorobenzene (HCB) on infant growth in the two first years of life.MethodsHCB was measured in breast milk samples in 449 mother-child pairs participating in the Norwegian birth cohort study HUMIS. We used these concentrations, mother's weight, height and age, together with child's weight at 8 age points, and proportion of milk consumed each month, to calculate HCB concentrations in the infant over age. We then estimated the association between HCB and infant growth using a linear mixed model.ResultsChildren exposed to HCB via mother's milk reached concentrations 1–5 times higher than the mother. HCB was associated with lower weight gain in the first 2 years (− 33 g per unit HCB and month, 95% CI: − 38, − 27 at 6 months). Associations were stronger during the first 3 months (− 57 g per unit HCB and month, 95% CI: − 67, − 49 at 1 month), indicating a critical window of effect. Our equations gave more precise estimates than the LEM.ConclusionOur equations for postnatal exposure of lipophilic environmental toxicants give better results than the LEM and are easier to implement than the complex PBPK models. HCB exposure, especially during the first three months of life, has a negative effect on infant growth up to 2 years.  相似文献   

11.
BackgroundATP-binding cassette (ABC) transporters have been associated with methylmercury (MeHg) toxicity in experimental animal models.AimsTo evaluate the association of single nucleotide polymorphisms (SNPs) in maternal ABC transporter genes with 1) maternal hair MeHg concentrations during pregnancy and 2) child neurodevelopmental outcomes.Materials and methodsNutrition Cohort 2 (NC2) is an observational mother-child cohort recruited in the Republic of Seychelles from 2008–2011. Total mercury (Hg) was measured in maternal hair growing during pregnancy as a biomarker for prenatal MeHg exposure (N = 1313) (mean 3.9 ppm). Infants completed developmental assessments by Bayley Scales of Infant Development II (BSID-II) at 20 months of age (N = 1331). Genotyping for fifteen SNPs in ABCC1, ABCC2 and ABCB1 was performed for the mothers.ResultsSeven of fifteen ABC SNPs (ABCC1 rs11075290, rs212093, and rs215088; ABCC2 rs717620; ABCB1 rs10276499, rs1202169, and rs2032582) were associated with concentrations of maternal hair Hg (p < 0.001 to 0.013). One SNP (ABCC1 rs11075290) was also significantly associated with neurodevelopment; children born to mothers with rs11075290 CC genotype (mean hair Hg 3.6 ppm) scored on average 2 points lower on the Mental Development Index (MDI) and 3 points lower on the Psychomotor Development Index (PDI) than children born to mothers with TT genotype (mean hair Hg 4.7 ppm) while children with the CT genotype (mean hair Hg 4.0 ppm) had intermediate BSID scores.DiscussionGenetic variation in ABC transporter genes was associated with maternal hair Hg concentrations. The implications for MeHg dose in the developing child and neurodevelopmental outcomes need to be further investigated.  相似文献   

12.
Although pesticide use is widespread in China, little is known about levels of exposure to organophosphate pesticides in the population and its potential adverse health effects. We investigated levels of organophosphate exposure in pregnant women and the association between organophosphate exposure and perinatal outcomes in Shanghai, China, by enrolling 187 healthy pregnant women between September 2006 and January 2007. Pesticide exposure was assessed by a questionnaire administered to the mothers in the hospital after delivery as well as by analyses of maternal urinary nonspecific metabolites of organophosphate pesticides (dimethyl and diethyl phosphates). Information on birth weight and length was collected from medical records. Geometric means of metabolites were 25.75 μg/L for dimethylphosphate (DMP); 11.99 μg/L for dimethylthiophosphate (DMTP); 9.03 μg/L for diethylphosphate (DEP); and 9.45 μg/L for diethyldithiophosphate (DETP). We found that a log unit increase in urinary DEP was associated with a decrease in gestational duration in girls by 1.79 weeks. [ßadjusted =  1.79 weeks per log10 unit increase; 95% confidence interval (CI), −2.82 to − 0.76; p = 0.001]. These data suggest that high pesticide level might adversely affect duration of gestation although this association was not present among boys. No associations for any of the organophosphate exposure measures were present for birth weight and length, suggesting that organophosphate pesticides may have no effects on fetal growth. Given that maternal urine pesticide levels in Shanghai were much higher than those reported in developed countries, more studies on the effects of in utero organophosphate exposure on fetal growth and child neurodevelopment are warranted.  相似文献   

13.
BackgroundBackground exposure to organochlorine (OC) pesticides was recently linked to cognitive impairment and dementia in cross-sectional and case–control studies. This prospective study was performed to evaluate if OC pesticides at baseline are associated with the future risk of cognitive impairment in elderly, with particular focus on weight change.MethodsPlasma concentrations of 3 OC pesticides (p,p′-DDE, trans-nonachlor, and hexachlorobenzene) were measured among 989 men and women aged 70 years in the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS). Cognitive impairment was validated by reviewing medical records. During the ten year follow-up, cognitive impairment was developed in 75 subjects. When weight change from age 70 to 75 was considered in analyses, elderly with incident cases before age 75 were excluded to keep the prospective perspective, leaving 795 study subjects and 44 incident cases.ResultsThe summary measure of 3 OC pesticides predicted the development of cognitive impairment after adjusting for covariates, including weight change. Compared to subjects with OC pesticides < 25th percentile, adjusted hazard ratios (HRs) in those with 25th–<75th and ≥ 75th percentiles were 3.5 (95% confidence interval: 1.5–8.5) and 3.2 (1.1–7.6), respectively (Ptrend = 0.04). Among 506 subjects who maintained or gained body weight, adjusted HRs were 6.9 and 11.6 (1.4–92.6) among the elderly in the 25th–<75th and ≥ 75th percentiles compared to < 25th percentile (Ptrend < 0.01).ConclusionsThis prospective study demonstrates that background exposure to OC pesticides are linked to the risk of developing cognitive impairment in elderly. The role of the chronic exposure to low dose OC pesticides in the development of dementia should be further evaluated in other populations.  相似文献   

14.
There is little evidence about exposure to currently used insecticides during early life periods and adverse effects on child neuropsychological development. The aim of this study is to examine the association between residential insecticide use during pregnancy and infancy, and the development of children.Study subjects were participants in the INMA (Environment and Childhood) Project, a Spanish multicenter birth cohort study. Prenatal and postnatal use of indoor insecticides and other variables were obtained from personal interview during pregnancy and infancy. Mental and psychomotor development was assessed around 14 months using the Bayley Scales of Infant Development. The associations were analyzed by linear regression models.54% of women used indoor insecticides at home during pregnancy and 47% postnatally. 34% of women used insecticide sprays and 33% used plug-in devices during pregnancy. During infancy, the percentage of women who used insecticide sprays decreased (22%), but the use of plug-in devices was similar to the prenatal period (32%). The use of insecticide sprays during pregnancy was associated with a decrement in psychomotor development (β =  1.9; 95%CI: − 3.4, − 0.5) but postnatal use did not associate with mental and psychomotor development. The negative effect was enhanced according to some modifying factors, such as being female, higher levels of prenatal exposure to PCB and mercury and belonging to the lowest social class.We found certain evidence about the adverse effect of using insecticide sprays during pregnancy on the psychomotor development of children. Some socio-demographic factors and other exposures could enhance that effect.  相似文献   

15.
BackgroundIndustrial plants emit air pollutants like fine particles (PM2.5), sulfur dioxide (SO2) and nitrogen dioxide (NO2) that may affect the health of individuals living nearby.ObjectiveTo assess the effects of community exposure to air emissions of PM2.5, SO2, and NO2 from pulp mills, oil refineries, metal smelters, on respiratory hospital admissions in young children in Quebec (QC) and British Columbia (BC), Canada.MethodsWe assessed QC, BC and pooled associations between the following estimates of exposure and hospital admissions for asthma and bronchiolitis in children aged 2–4 years for the years 2002–2010: i) Crude emission exposures at the residential postal codes of children, calculated by multiplying estimated daily emissions of PM2.5, SO2, or NO2 from all nearby (< 7.5 km) pulp mills, oil refineries, metal smelters emitting yearly ≥ 50 t and their total emissions, by the percent of the day each postal code was downwind; ii) Daily levels of these pollutants at central ambient monitoring stations nearby the industries and the children's residences.ResultsSeventy-one major industries were selected between QC and BC, with a total of 2868 cases included in our analyses. More cases were exposed to emissions from major industries in QC than in BC (e.g. 2505 admissions near SO2 industrial emitters in QC vs 334 in BC), although air pollutant levels were similar. Odds ratios (ORs) for crude refinery and smelter emissions were positive in QC but more variable in BC. For example with PM2.5 in QC, ORs were 1.13 per 0.15 t/day (95% CI: 1.00–1.27) and 1.03 (95% CI: 0.99–1.07) for refinery and smelter emissions, respectively. Pooled results of QC and BC for crude total SO2 emissions from all sources indicated a 1% increase (0–3%) in odds of hospital admissions per 1.50 t/day increase in exposure. Associations with measured pollutant levels were only seen in BC, with SO2 and NO2.ConclusionHospital admissions for wheezing diseases in young children were associated with community exposure to industrial air pollutant emissions. Future work is needed to better assess the risk of exposure to complex mixture of air pollutants from multiple industrial sources.  相似文献   

16.
BackgroundAssociations of ambient air pollutants with respiratory health are inconsistent.ObjectivesWe analyzed the associations of gestational and early life exposures to air pollutants with doctor-diagnosed asthma, allergic rhinitis, and pneumonia in children.MethodsWe selected 3358 preschool children who did not alter residences after birth from a cross-sectional study in 2011–2012 in Shanghai, China. Parents reported children's respiratory health history, home environment, and family lifestyle behaviors. We collected daily concentrations of sulphur dioxide (SO2), nitrogen dioxide (NO2), and particulate matter with an aerodynamic diameter ≤ 10 μm (PM10) during the child's total lifetime (2006–2012) for each district where the children lived. We analyzed the associations using logistic regression models.ResultsAfter adjusting for covariates and the other studied pollutants, we found that exposure to NO2 (increment of 20 μg/m3) during the first year of life was significantly associated with asthma [odds ratio (OR) = 1.77; 95% confidence interval (CI): 1.29–2.43] and allergic rhinitis (OR = 1.67; 95% CI: 1.07–2.61). Exposure to NO2 during gestation, the first two and three years, and over total lifetimewas all consistently associated with increased odds of allergic rhinitis. Quartiles of NO2 concentration during different exposure periods showed a slight dose–response relationship with the studied diseases. These diseases had significant associations with pollutant mixtures that included NO2, but had no significant association with exposures to SO2 and PM10 individually or in mixtures.ConclusionsGestational and early life exposures to ambient NO2 are risk factors for childhood respiratory diseases.  相似文献   

17.
BackgroundShort telomeres are associated with chronic disease and early mortality. Recent studies in adults suggest an association between telomere length and exposure to particulate matter, and that ethnicity may modify the relationship. However associations in children are unknown.ObjectivesWe examined associations between air pollution and telomere length in an ethnically diverse group of children exposed to high levels of traffic derived pollutants, particularly diesel exhaust, and to environmental tobacco smoke.MethodsOral DNA from 333 children (8–9 years) participating in a study on air quality and respiratory health in 23 inner city London schools was analysed for relative telomere length using monochrome multiplex qPCR. Annual, weekly and daily exposures to nitrogen oxides and particulate matter were obtained from urban dispersion models (2008–10) and tobacco smoke by urinary cotinine. Ethnicity was assessed by self-report and continental ancestry by analysis of 28 random genomic markers. We used linear mixed effects models to examine associations with telomere length.ResultsTelomere length increased with increasing annual exposure to NOx (model coefficient 0.003, [0.001, 0.005], p < 0.001), NO2 (0.009 [0.004, 0.015], p < 0.001), PM2.5 (0.041, [0.020, 0.063], p < 0.001) and PM10 (0.096, [0.044, 0.149], p < 0.001). There was no association with environmental tobacco smoke. Telomere length was increased in children reporting black ethnicity (22% [95% CI 10%, 36%], p < 0.001)ConclusionsPollution exposure is associated with longer telomeres in children and genetic ancestry is an important determinant of telomere length. Further studies should investigate both short and long-term associations between pollutant exposure and telomeres in childhood and assess underlying mechanisms.  相似文献   

18.
BackgroundA major threat to public health involving phthalate-tainted foodstuffs occurred in Taiwan in 2011. Phthalates, mainly di-(2-ethylhexyl) phthalate (DEHP), were intentionally added to several categories of food commonly consumed by children. This study investigated the relationship between intake of the phthalate-tainted foods and renal function in children.MethodsChildren aged ≤ 10 years with possible phthalate exposure were enrolled in this study between August 2012 and January 2013. Questionnaires were used to collect details of exposure to phthalate-tainted foodstuffs, and blood and urine samples were collected for clinical biochemical workup. The clinical biomarkers of renal injury, including urinary microalbumin, N-acetyl-beta-d-glucosaminidase (NAG), and β2-microglobulin were measured. Exposure was categorized based on recommended tolerable daily intake level defined by the U.S. Environmental Protection Agency (0.02 mg/kg/day) and the European Food Safety Authority (0.05 mg/kg/day).ResultsWe analyzed intake and renal function of 184 children whose intake of DEHP-tainted foods was known. Higher DEHP exposure to DEHP-tainted foods was significantly associated with increase of urine albumin/creatinine ratio (ACR). Children in the high-exposed group (daily DEHP intake (DDI) > 0.05 mg/kg/day) had 10.395 times the risk of microalbuminuria than the low-exposed group (DDI  0.02 and > 0 mg/kg/day) and no-exposed group combined after adjustment (95% CI = 1.096–98.580, P = 0.04).ConclusionIntake of DEHP from phthalate-tainted foods may be a potential risk factor for microalbuminuria, a marker of glomerular injury in children.  相似文献   

19.
BackgroundThe aim of this study is to investigate whether memory performance in adolescents is affected by radiofrequency electromagnetic fields (RF-EMF) from wireless device use or by the wireless device use itself due to non-radiation related factors in that context.MethodsWe conducted a prospective cohort study with 439 adolescents. Verbal and figural memory tasks at baseline and after one year were completed using a standardized, computerized cognitive test battery. Use of wireless devices was inquired by questionnaire and operator recorded mobile phone use data was obtained for a subgroup of 234 adolescents.RF-EMF dose measures considering various factors affecting RF-EMF exposure were computed for the brain and the whole body.Data were analysed using a longitudinal approach, to investigate whether cumulative exposure over one year was related to changes in memory performance. All analyses were adjusted for relevant confounders.ResultsThe kappa coefficients between cumulative mobile phone call duration and RF-EMF brain and whole body dose were 0.62 and 0.67, respectively for the whole sample and 0.48 and 0.28, respectively for the sample with operator data. In linear exposure–response models an interquartile increase in cumulative operator recorded mobile phone call duration was associated with a decrease in figural memory performance score by − 0.15 (95% CI: − 0.33, 0.03) units. For cumulative RF-EMF brain and whole body dose corresponding decreases in figural memory scores were − 0.26 (95% CI: − 0.42, − 0.10) and − 0.40 (95% CI: − 0.79, − 0.01), respectively. No exposure-response associations were observed for sending text messages and duration of gaming, which produces tiny RF-EMF emissions.ConclusionsA change in memory performance over one year was negatively associated with cumulative duration of wireless phone use and more strongly with RF-EMF dose. This may indicate that RF-EMF exposure affects memory performance.  相似文献   

20.
Ambient air pollution and children's lung function in China   总被引:1,自引:0,他引:1  
ObjectiveTo describe the correlations between ambient air pollutants (TSP, SO2, NOx) and the level of children's lung function (FVC, FEV1, MMEF) in China.MethodsWe collected the research articles on ambient air pollution and children's lung function published from 1985 to 2006 and selected 11 articles finally according to the following criteria: (1) Children between the age of 7 and 15 as objects; (2) Local air quality monitoring results were reported; (3) Strict quality control was taken when testing children's lung function; (4) The results were expressed by the average of measured value. Then we analyzed the correlation relationship between the level of ambient air pollutants and children's lung function and compared the effects of ambient air pollutants on children's lung function of boy and girl.ResultsThe selected articles included the results of 7 cities in China. Among them, the results of 6 cities' studies revealed that the levels of children's lung function were significantly lower in the areas with heavy ambient air pollution than those in the areas with light ambient air pollution. According to the articles, the average levels of TSP were at the range of 0.084 mg/m3–0.835 mg/m3, SO2 were 0.013 mg/m3–0.929 mg/m3, NOx were 0.044 mg/m3–0.229 mg/m3. Correlation analysis showed significant negative correlation between the levels of TSP and SO2 and children's FVC and FEV1, as well as the levels of NOx and children's MMEF. The correlation coefficient was ? 0.797 (t = ? 4.384, P = 0.001) between TSP and FVC, ? 0.693 (t = ? 4.190, P < 0.001) between Ln (SO2) and FVC, ? 0.886 (t = ? 5.392, P = 0.001) and ? 0.685 (t = ? 4.101, P = 0.001) between FEV1 and TSP and Ln (SO2), and ? 0.973 (t = ? 5.993, P = 0.027) between NOxNOx and MMEF, respectively. The results also suggested that the decreases of lung function for girl with the increasing of ambient air pollution were significantly greater for boy.ConclusionThe levels of ambient air TSP and SO2 correlated with the damage of the big airway function of children, while NOxNOx affected the small airway function chiefly. Furthermore, lung function of girl was more susceptible to ambient air pollutants than boy.  相似文献   

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