Early Childhood Exposure Research Articles

19 Maternal and early childhood exposures in relation to juvenile idiopathic arthritis

Abstract Background Juvenile idiopathic arthritis (JIA) is the most common rheumatic disease in children. JIA likely has a complex aetiology, with multiple genetic and environmental factors contributing to its development. Existing data on associations between maternal and early childhood exposures and JIA is rare. Previous studies showed potential role for prematurity, number of siblings and infections. Objectives The aim of our study is to assess maternal and early childhood exposures in patients with JIA. Methods Mothers of children with JIA followed in rheumatology department were asked about maternity related data as well as the course of perinatal period of the child with JIA based on the International League of Associations for Rheumatology (ILAR) criteria. Exposure information from birth included: Maternal factors (age when they had the first child, age when they had the child with JIA, plurality (singleton, twin/multiple gestation), number of prior fetal losses, number of prior births; delivery method (vaginal, cesarean section)) and also information about birth weight (low (<2500 grams), normal (2500– 4000 grams), excessive (4000+ grams)); size for- gestational-age and gestational age (preterm, normal term, post term) and postpartum complications. Results Thirty children (sixteen females and fourteen males) with JIA were included. The most common type of JIA was enthesitis-related in 13 cases, then oligoarthritis in 8 cases, polyarthritis without rheumatoid factor in 4 cases, polyarthritis with positive rheumatoid factor in 2 cases and psoriatic arthritis in 3 cases. The mean age of the mothers was 27.1 years [22–40] when they had their first child and 30.27 years [22–42] when they had their child with JIA. They were nulliparous in 40% of the cases. All of the children were from a singleton pregnancy. Thirty percent of the mothers had at least one prior fetal loss before they had their child with JIA. During their pregnancy with their child with JIA, five mothers had pre-eclampsia and two of them had gestational diabetes. None of them smoked during the pregnancy. Only 2 children had preterm birth. Birth weight was normal (2.500–4.000 grams) in 24 cases, low in 3 cases (<2.500 grams) and above normal (>4000 grams) in 3 cases. Size for gestational age was normal in all cases. Nineteen mothers had vaginal delivery and eleven had cesarean section. Neonatal complications were noted in 7 cases who needed to be admitted to neonatal intensive care unit (1 for hypoglycemia, 1 for jaundice, 2 for infection, 1 for respiratory distress and two because of preterm birth). Maternal complications were noted in four cases: 2 postpartum hemorrhage and 2 postpartum infections. Conclusion Our study assessed maternal and early childhood exposures in patients with JIA. Further studies are required to explore associations between these factors and the occurrence of the disease for a better knowledge of etiologies of JIA and for a possible prevention from this pathology.

Chinese famine exposure in early life and metabolic obesity phenotype in middle age: Results from the China health and retirement longitudinal study.

ObjectiveTo assess the association between early life exposure to famine and the risk of metabolic obesity phenotypes among adults in middle age.MethodsThe study selected two comparison groups. Comparison A consisted of a non-exposed group born between 1963-1965 from the China Health and Retirement Longitudinal Study (CHARLS) 2015 wave (N=862) and a fetal-exposed group born between 1959-1961 from the 2011 wave (N=507). Comparison B consisted of an early childhood-exposed group born between 1955-1957 from the 2011 wave (N=830) and a fetal-exposed group born between 1959-1961 from the 2015 wave (N=552). Multivariable logistic regressions were conducted to explore the associations between different periods of famine exposure and obesity, metabolic health status, and metabolic obesity phenotypes, with stratification by sex.ResultsCompared with the non-exposed group, participants exposed to famine in the fetal period had a significantly lower risk of overweight/obesity (OR: 0.78, 95%CI: 0.63-0.97) and a higher risk of metabolically unhealthy status (OR: 1.73, 95%CI: 1.34-2.23) and metabolically unhealthy non-obesity (MUNO) (OR: 2.12, 95%CI: 1.46-3.08) at the age of 50-52 years. In the sex-stratified analysis, males exposed to famine in the fetal period had a significantly lower risk of overweight/obesity (OR: 0.59, 95%CI: 0.43-0.80) and metabolically healthy obesity (MHO) (OR: 0.56, 95%CI: 0.37-0.85), while such associations were not found in females. Compared with the early childhood exposure group, participants in the fetal exposure group had a significantly lower risk of metabolic unhealthy status (OR: 0.65, 95%CI: 0.51-0.85) and MUNO (OR: 0.50, 95%CI: 0.35-0.72). Those associations were observed in both males and females.ConclusionExposure to famine in early life increased the risk of metabolically unhealthy status in adulthood. Different metabolic subtypes should be identified at an early stage and followed by classification, intervention, and treatment.

Effects of Early Childhood Exposure to Pollution on Crime: Evidence from 1970 Clean Air Act

Past literature has shown that 1970 amendments to the clean air act (CAA) led to significant reduction in air pollution early 1970s, and that it had positive infant health consequences for the cohorts treated by CAA. Because effects of in-utero and early childhood conditions are persistent, and the health effects can remain latent for years, CAA may impact the future adult outcomes. In this paper, I investigate the impact of the CAA on the future crime. In a difference-in-differences framework, I find that the cohorts that were born in the year of the CAA’s first implementation commit fewer crimes 15–24 years later. The magnitude of this impact is about 6%. Property crimes rather than violent crimes are impacted. I also estimate that CAA reduced the ambient air pollution by 17%. These reduced form estimates suggest that a 1% reduction in air pollution reduces future crime rate by 0.35%.

Review of evaluation methods for maltreatment exposure in early childhood

儿童早期（0~6岁）对个体发展至关重要，而这段时期恰恰是儿童虐待最容易发生的时期。评估儿童早期虐待的方法主要有父母报告、专业人员评估、机构报告以及通过头发皮质醇的测量来评估儿童的压力暴露从而推测可能的虐待风险等。本综述从人群研究角度对现有0~6岁儿童虐待的评估方法进行阐述，以期为今后开展相关研究提供方法学参考。.

Epilepsy in children exposed to family and domestic violence in the first 5 years of life.

To investigate childhood (0-18 years) hospitalisation and emergency department (ED) contacts for epilepsy in Western Australian (WA) children exposed to family and domestic violence (FDV) pre 5 years of age compared to children with no FDV exposure. A retrospective, population-based cohort study included children born 1987-2010 who were identified as being exposed to FDV (n=7018) from two sources: WA Police Information Management System and WA Hospital Morbidity Data Collection (HMDC) and a non-exposed comparison group (n=41 996). Epilepsy contact was identified in HMDC and ED Data Collection records. Cox regression was used to estimate the adjusted and unadjusted hazard ratio and 95% confidence interval (CI) for epilepsy contact; adjustment was made for a range of demographic characteristics known to impact health outcomes. Analyses were stratified by Aboriginal and Torres Strait Islander status to account for higher rates of FDV and epilepsy hospital admissions in Aboriginal and Torres Strait Islander children. Children exposed to FDV had a 62% (HR 1.62, 95% CI: 1.33-1.98) increased risk of epilepsy contact than non-exposed counterparts. Furthermore, the children exposed to FDV had a 50% longer average hospital stay for epilepsy than non-exposed children (4.7 days vs. 3 days, P=0.006). When stratified by Aboriginal status, we found that Aboriginal children exposed to FDV stayed (on average) 2 days longer in hospital for epilepsy than their non-exposed counterparts (5.1 days vs. 3.1 days, P=0.018). FDV exposure in early childhood is associated with increased risk of requiring secondary health care and longer hospital stays for childhood epilepsy.

Early Childhood Exposure to Intimate Partner Violence and Developmental Vulnerability at Kindergarten: Linking Canadian Population-Level Administrative Data.

ObjectiveThe objective was to examine the relationship between maternal intimate partner violence (IPV) victimization and children’s developmental health using linked population-wide administrative datasets. We examined developmental vulnerability (DV) at kindergarten of children exposed to maternal IPV victimization aged 0 to 5 using provincial prosecution records compared to unexposed counterparts. ApproachThis retrospective cohort study linked administrative datasets (legal, health, education, social services) from the Population Research Data Repository at the Manitoba Centre for Health Policy. Exposed mother-child pairs with 1+ prosecution records of maternal IPV victimization during early childhood (child aged 0 to 5) between 2003-2018 in Manitoba (n = 5,728) were matched to unexposed pairs (1:3) based on sex/birthdate of child and neighbourhood income. DV at kindergarten was measured across 5 domains (physical, social, emotional, language/cognitive [LC], communication/general knowledge) using the Early Developmental Instrument (EDI). Children without eligible EDI scores were excluded. Multiple logistic regression models were conducted. ResultsThe cohort included 5321 children (exposed n=1365, unexposed n=3956). 32.98% of the cohort was developmentally vulnerable in one or more domains (1/+) and 19.60% was developmentally vulnerable in two or more domains (2/+). Unadjusted relationships between maternal IPV victimization from age 0 to 5 and developmental vulnerability at kindergarten were statistically significant across all 5 domains (e.g., LC OR=2.76 [2.36, 3.23]) and in 1/+ (OR=2.72 [2.39, 3.09]) as well as 2/+ (OR=2.89 [2.51, 3.34]) domains. After adjusting for covariates, children who were exposed to maternal IPV victimization from ages 0 to 5 had increased odds of being developmentally vulnerable in social competence (aOR=1.33 [1.07, 1.66]) and emotional maturity (aOR=1.29 [1.03, 1.62]), also in 2/+ domains (aOR=1.42 [1.15, 1.73]) at kindergarten, compared to unexposed counterparts. ConclusionThe study provided Canadian population-wide evidence of the association between maternal IPV victimization and early childhood development, specifically later socio-emotional vulnerability. Interventions and support systems for this population of families should be developed and implemented, with an emphasis on mitigating long-term socio-emotional developmental risks in children exposed to IPV.

Early-life exposure to tobacco and childhood adiposity: Identifying windows of susceptibility.

Early-life exposure to tobacco is associated with obesity, but the most susceptible developmental periods are unknown. To explore windows of susceptibility in a cohort of 568 mother-child pairs. We measured seven measures of tobacco exposure (five self-reported and two biomarkers) spanning from pre-conception to age 5 years. Mothers self-reported active smoking (pre-conception, 17 weeks, and delivery) and household smokers (5 and 18 months postnatally). Cotinine was measured in maternal urine (27 weeks) and child urine (5 years). Adiposity (fat mass percentage) was measured at birth and 5 years via air displacement plethysmography. Using a multiple informant approach, we tested whether adiposity (5 years) and changes in adiposity (from birth to 5 years) differed by the seven measures of tobacco exposure. The associations may depend on timing. For example, only pre-conception (β=3.1%; 95% CI: 1.0-5.1) and late gestation (β=4.0%; 95% CI: 0.4-7.6) exposures influenced adiposity accretion from birth to 5 years (p for interaction=0.01). Early infancy exposure was also associated with 1.7% higher adiposity at 5 years (95% CI: 0.1-3.2). Mid-pregnancy and early childhood exposures did not influence adiposity. Pre-conception, late gestation, and early infancy exposures to tobacco may have the greatest impact on childhood adiposity.

Exposure to Intimate Partner Violence in Children Aged 6 Months to 8 Years: Factors Associated with Mothers' Awareness of Children's Exposure to This Violence

Early childhood exposure to intimate partner violence (EIPV) is a serious social and public health matter. Parents underestimate EIPV in comparison to their own victimization of intimate partner violence (IPV). However, few studies have attempted to compare the differences between the child's EIPV and the IPV victimization from the mothers' perspective and document the associated explanatory factors. Consequently, this study was conducted on a representative sample of 2046 children aged 6 months to 8 years in Quebec (Canada) to estimate the prevalence of EIPV and mother's awareness of EIPV over the past 12 months and to investigate factors that are associated with mother's awareness of EIPV. Findings revealed that 11.1% of young children were exposed to at least one form of IPV. However, that proportion decreases to 5.9% when the mother is asked whether the child is aware or a witness of the violence. Regression analyses revealed that child's younger age, mother's depressive symptoms, being a single parent, and the presence of adults' violent behaviors toward children were significantly associated with the mother's higher perceived awareness of EIPV. While some of these findings are consistent with previous studies, others such as living in a single-parent family open the door to different interpretations, including the presence of increased postseparation violence. As EIPV is increasingly recognized as affecting children regardless of their awareness of violent events, further studies are needed to better understand the context facilitating parental recognition of this exposure.

Elements That Influence the Development of Attention Deficit Hyperactivity Disorder (ADHD) in Children.

Various factors may have a role in the development of attention deficit hyperactivity disorder (ADHD). Although the specific pathophysiology of this disease is still not entirely understood, it is believed to be caused by a mix of genetic, maternal, dietary, and environmental factors. The effect of these factors can determine the severity of ADHD; for example, some of them are dose-dependent, but there is a typical pattern that all are known to be associated with either early childhood exposure or maternal exposure during pregnancy. Some factors share a similar mechanism of affecting pathways and increasing the risk of ADHD.ADHD is not a disorder that can be detected before symptoms appear in a child, making it more challenging to anticipate even if a child has been exposed to a known trigger. Environmental pollutants were investigated, and it was shown that there was a link between ADHD in childhood and exposure to pollutants throughout childhood or during pregnancy. It is well known that maternal health is a significant factor in the unborn child's development in many health aspects. The central nervous system (CNS) is a primary system that can suffer irreversible damage from health conditions, stress, depression, or specific nutritional deficiency when the pregnant mother is subjected to these conditions. Even though numerous studies have been conducted to investigate the probable causes of ADHD, with some of them having robust findings, no conclusive explanation can be provided to identify a definitive cause or a risk factor.

Health Outcomes in Children Associated with Prenatal and Early-Life Exposures to Air Pollution: A Narrative Review.

(1) Background: The developmental origins of health and disease (DOHaD) hypothesis links adverse fetal exposures with developmental mal-adaptations and morbidity later in life. Short- and long-term exposures to air pollutants are known contributors to health outcomes; however, the potential for developmental health effects of air pollution exposures during gestation or early-childhood have yet to be reviewed and synthesized from a DOHaD lens. The objective of this study is to summarize the literature on cardiovascular and metabolic, respiratory, allergic, and neuropsychological health outcomes, from prenatal development through early childhood, associated with early-life exposures to outdoor air pollutants, including traffic-related and wildfire-generated air pollutants. (2) Methods: We conducted a search using PubMed and the references of articles previously known to the authors. We selected papers that investigated health outcomes during fetal or childhood development in association with early-life ambient or source-specific air pollution exposure. (3) Results: The current literature reports that prenatal and early-childhood exposures to ambient and traffic-related air pollutants are associated with a range of adverse outcomes in early life, including cardiovascular and metabolic, respiratory and allergic, and neurodevelopmental outcomes. Very few studies have investigated associations between wildfire-related air pollution exposure and health outcomes during prenatal, postnatal, or childhood development. (4) Conclusion: Evidence from January 2000 to January 2022 supports a role for prenatal and early-childhood air pollution exposures adversely affecting health outcomes during development. Future studies are needed to identify both detrimental air pollutants from the exposure mixture and critical exposure time periods, investigate emerging exposure sources such as wildfire, and develop feasible interventional tools.

Association between Early Life Famine Exposure and Metabolic Syndrome in Adulthood.

To analyze the relationship between famine exposure at different stages of early life and the risk of developing metabolic syndrome (MetS) in adulthood, 11,865 study participants from the 2015 Chinese Adult Chronic Disease and Nutrition Surveillance Program were enrolled and then divided into a non-exposed group, fetal exposure group, early childhood exposure group, middle childhood exposure group and late childhood exposure group according to their birth time and famine exposure. MetS was defined by the NCEP ATP III criteria. Using logistic regression to explore the association between famine exposure at different stages of early life and the increased risk of developing MetS in adulthood. After adjusting other factors, compared with the non-exposure group, famine exposure during the fetal period (OR = 1.23, 95% CI = 1.00–1.51), early childhood (OR = 1.44, 95% CI = 1.11–1.87), middle childhood (OR = 1.50, 95% CI = 1.13–1.99) and late childhood (OR = 1.67, 95% CI = 1.21–2.30) had a higher risk of developing MetS in adulthood. Stratified analysis found an association between early life famine exposure and the increased risk of MetS in adulthood in females, overweight or obese participants and those who lived in areas of severe famine, in city areas and in southern China. Compared with the non-exposed group, the fetal, early childhood, middle childhood and late childhood famine-exposed groups are more likely to suffer from MetS in adulthood, especially the subjects who are females, overweight or obese and had lived in severe famine areas, city areas and southern China.

Early childhood exposure to health insurance and adolescent outcomes: Evidence from rural China

This paper examines the impact of exposure to public health insurance in early life on outcomes in adolescence in rural China. Exploiting the variation in the county-by-county rollout of the New Cooperative Medical Scheme (NCMS) between 2003 and 2008, we find that exposure to the NCMS during ages 0–5 significantly improves health, cognitive, and educational outcomes during adolescence. In contrast, exposure after age five has no significant effects. Our further investigation provides evidence for several underlying mechanisms, such as improved prenatal care and birth outcomes, better preventive medical protection against childhood diseases, and lower risk in medical expenditure. (JEL Classification I13; I21; D04).

Low level lead exposure in early childhood and parental education on adolescent IQ and working memory: a cohort study.

The independent effect of lead exposure and parental education on children's neurocognition is well-documented. However, few studies have examined the combined effect of childhood lead exposure and parental education on adolescent neurocognition, especially in China. Examine both the combined and interactive effect of childhood blood lead levels (BLLs) and parental education on early adolescent neurocognition. 417 children from a longitudinal cohort study in Jintan, China had BLLs measured at 3-5 years and 12 years, parental education levels assessed at 3-5 years, and neurocognitive outcomes tested at 12 years. BLLs at 3-5 years were inversely associated with adolescent IQ (β -0.55 95% CI: -0.97, -0.13) but not working memory (β -0.06 95% CI: -0.23, 0.11) and parental education was positively associated with adolescent IQ (β 0.68 95% CI: 0.19, 1.17) and working memory (β 0.24 95% CI: 0.04, 0.44). BLLs and parental education evidenced combined effects on neurocognition, where children with higher BLLs and lower fathers' education had mean IQ scores 7.84 (95% CI: -13.15, -2.53) points lower than children with lower BLLs and higher fathers' education. There were significant associations between parental education and working memory, however, not with BLLs. The interaction between mother and father high school education and BLLs was insignificant for effects on IQ and working memory. Childhood lead exposure and parental education levels have a combined and long-term impact on IQ, evidence that may partially explain disparities in lead exposure associated outcomes and highlight those children at greatest risk for neurocognitive deficits. Children continue to be exposed to low-levels of environmental lead in China and globally, warranting examination of the impact of such exposures. This paper demonstrates that even relatively low-level lead exposure in early childhood significantly influences adolescent neurocognitive functioning. Furthermore, co-existing social determinant of health-related variables, measured here as parental education, have a combined impact on neurocognition. These results highlight children at greater risk for neurocognitive deficits and demonstrate the need to examine the influence of lead exposure within the broader socio- ecological environment, as these factors work in tandem to influence longer-term neurocognitive outcomes.

Early life exposure to the Chinese Famine of 1959-1961 is an independent risk factor of adulthood elevated homocysteine, hyperuricemia, high LDL, and hypertension.

Famine exposure in early life was associated with cardiovascular diseases in later life. Whether biochemical surrogates of cardiovascular diseases, such as homocysteine and uric acid, are also associated with famine exposure is unknown so far. Data were derived from a population-based cross-sectional study in the Hunan Province of China, which was heavily affected by the Famine in 1959-1961. A total of 1,150 adults born between 1952and1964 were selected, and 5 cohorts were defined: no exposure, fetal, early childhood, mid-childhood, and late childhood exposure. Compared with the no-famine exposure group, participants exposed to famine in their fetal period had a higher risk of high homocysteine in adulthood with OR of 2.21 (95% CI: 1.01-4.83), whereas famine exposures in early, mid, or late childhood were not significantly associated with high homocysteine in adulthood. Similarly, participants in the fetal famine exposure group had a 1.59-fold higher risk of hyperuricemia (OR = 2.59, 95% CI: 1.07-5.30) and a 2.03-fold higher risk of high low-density lipoprotein cholesterol (LDL) (OR = 0.03, 95% CI: 1.35-6.78) in adulthood compared to those without famine exposure, respectively. We furthermore conducted a meta-analysis including 16 studies regarding the association between fetal famine exposure and adulthood hypertension, including our study. The meta-analysis, including 34,804, subjects showed that fetal famine exposure is associated with a higher risk of adulthood hypertension (OR=1.22, 95% CI: 1.07-1.40). Taken together, fetal famine exposure is related to higher odds of cardio-metabolic risk factors, such as high homocysteine, hyperuricemia, and LDL as well as hypertension, suggesting that undernutrition during fetal life may affect metabolism of homocysteine, uric acid, and LDL in adulthood.

Quantile regression to examine the association of air pollution with subclinical atherosclerosis in an adolescent population.

Air pollution has been associated with carotid intima-media thickness test (CIMT), a marker of subclinical atherosclerosis. To our knowledge, this is the first study to report an association between ambient air pollution and CIMT in a younger adolescent population. To investigate the associations beyond standard mean regression by using quantile regression to explore if associations occur at different percentiles of the CIMT distribution. We measured CIMT cross-sectionally at the age of 16years in 363 adolescents participating in the Dutch PIAMA birth cohort. We fit separate quantile regressions to examine whether the associations of annual averages of nitrogen dioxide (NO2), fine particulate matter (PM2.5), PM2.5 absorbance (a marker for black carbon), PMcoarse and ultrafine particles up to age 14 assigned at residential addresses with CIMT varied across deciles of CIMT. False discovery rate corrections (FDR, p<0.05 for statistical significance) were applied for multiple comparisons. We report quantile regression coefficients that correspond to an average change in CIMT (µm) associated with an interquartile range increase in the exposure. PM2.5 absorbance exposure at birth was statistically significantly (FDR<0.05) associated with a 6.23µm (95% CI: 0.15, 12.3) higher CIMT per IQR increment in PM2.5 absorbance in the 10th quantile of CIMT but was not significantly related to other deciles within the CIMT distribution. For NO2 exposure we found similar effect sizes to PM2.5 absorbance, but with much wider confidence intervals. PM2.5 exposure was weakly positively associated with CIMT while PMcoarse and ultrafine did not display any consistent patterns. Early childhood exposure to ambient air pollution was suggestively associated with the CIMT distribution during adolescence. Since CIMT increases with age, mitigation strategies to reduce traffic-related air pollution early in life could possibly delay atherosclerosis and subsequently CVD development later in life.

Early linguistic experience shapes bilingual adults\u2019 hearing for phonemes in both languages

English and Mandarin Chinese differ in the voice onset times (VOTs) of /b/ and /p/. Hence the way bilinguals perceive these sounds may show ‘tuning’ to the language-specific acoustic structure of a bilingual’s languages (a discrete model), or a shared representation across languages (a unitary model). We investigated whether an individual’s early childhood exposure influences their model of phoneme perception across languages, in a large sample of early English-Mandarin bilingual adults in Singapore (N = 66). As preregistered, we mapped identification functions on a /b/-/p/ VOT continuum in each language. Bilingual balance was estimated using principal components analysis and entered into GLMMs of phoneme boundary and slope. VOT boundaries were earlier for English than Mandarin, and bilingual balance predicted the slope of the transition between categories across both languages: Those who heard more English from an earlier age showed steeper category boundaries than those who heard more Mandarin, suggesting early bilinguals may transfer their model for how phonemes differ from their earlier/stronger languages to later/weaker languages. We describe the transfer model of discrete phoneme representations and its implications for use of the phoneme identification task in diverse populations.

The association of prenatal and childhood pyrethroid pesticide exposure with school-age ADHD traits.

Pyrethroid insecticides are commonly used in residential settings, and their use has increased rapidly. Although research has been scarce, they have been reported to be associated with impaired neurodevelopment. Moreover, susceptible exposure windows and the long-term effects of pyrethroids have not been investigated. We examined the association between pyrethroid exposure and attention-deficit/hyperactivity disorder (ADHD) symptoms over time, with exposure windows spanning from the prenatal period to school-age. Using 524 mother-child pairs, we measured urinary concentrations of 3-phenoxybenzoic acid (3-PBA), a major pyrethroid metabolite, and asked parents to fill-out the ADHD Rating Scale IV (ARS). We used Poisson regression to identify the susceptible periods of pyrethroid exposure, by correlating various 3-PBA exposure windows (prenatal, ages 2, 4, 6 and 8) with ADHD symptoms at ages 6 and 8. Doubling of prenatal and age 2 3-PBA concentrations was associated with increased ADHD symptoms at age 6 (2.7% change, 95% confidence interval [CI]: 0.3, 5.2; 5.2% change [95% CI: 0.5, 10.2], respectively). The 3-PBA concentrations at age 4 and age 6 were linked with ADHD symptoms at age 8 (2.7% change [95% CI: 0.3, 5.3]; 3.3% change [95% CI: 0.2, 6.4], respectively). There were no clear sex-specific patterns in association. Both prenatal and early-childhood exposure to 3-PBA were found to be associated with ADHD symptoms. Exposure during pregnancy, and at ages 2 to 6 were found to be susceptible periods for pyrethroid neurotoxicity at ages 6 and 8.

Association between fetal famine exposure and risk of type 2 diabetes: a prospective cohort study.

The objective of this study was to explore the effects of fetal experience of famine on the onset of type 2 diabetes mellitus (T2DM) in adults. The analysis included 16 594 participants from the Kailuan Study who were free of diabetes at baseline (2006). According to the date of birth, the individuals born on October 1, 1962- September 30, 1964, were divided into the non-exposed group (used as the reference group), individuals born on October 1, 1959- September 30, 1961, were divided into the fetal exposure group, and the early childhood exposure group included those born on October 1, 1956- September 30, 1958. The cumulative incidence of T2DM for each group was calculated and compared among the 3 groups, and the Cox regression model was used to analyze the effects of fetal famine experience on the risk of diabetes. During a median 10.27 years (170 358 person-years) (2006-2017), 3509 incident T2DM cases were identified, with a cumulative incidence rate of 19.46%. The cumulative incidences of T2DM in the non-exposed, fetal exposure, and early childhood exposure groups were 17.38%, 20.85%, and 20.65%, respectively (P < 0.01). After adjusting for confounding factors, the hazard ratio (HR) of T2DM in the fetal exposure group was 1.222 (95% confidence interval: 1.087-1.374, P < 0.01), compared with the reference group. The association was modified by sex and hypertension (both P interaction less than 0.05). Fetal famine exposure may increase the risk of developing T2DM in adults. This association was more pronounced among women and those with hypertension. Novelty: The association was modified by sex and hypertension. Long follow-up time.

Farm exposure and rates of early life respiratory illness and wheeze

Early childhood exposure to animal farming environments has been associated with decreased incidence of allergy and asthma. We hypothesize that children raised in Wisconsin farm environments will have a lower incidence of viral wheeze in the first two years of life.

Prenatal and early childhood exposure to tetrachloroethylene (PCE)-contaminated drinking water and sleep quality in adulthood: a retrospective cohort study

BackgroundCommunities in Cape Cod, Massachusetts were exposed to tetrachloroethylene (PCE) through contaminated drinking water from 1969 to 1983. PCE exposure during adulthood has well-established neurotoxic effects; however, long-term impacts stemming from early life exposure, especially adverse effects on sleep quality, are not well understood.MethodsThe present analysis was based on data from the Cape Cod Health Study, a retrospective cohort study of the long-term neurotoxic impacts of early-life exposure to PCE-contaminated drinking water. Exposure to PCE-contaminated water was estimated using a validated leaching and transport model. Measures of sleep quality were obtained from self-administered questionnaires. Generalized estimating equations were used to generate risk ratios and 95% confidence intervals to estimate the association between early-life PCE exposure and sleep quality among 604 participants.ResultsCompared to unexposed participants, any PCE exposure during early life was associated with 1.57 times the risk of reporting breathing pauses during sleep (95% CI 0.92–2.68). Low-level exposure to PCE was associated with 1.50 times the risk of reporting sleep apnea or other sleep disorders (95% CI 0.78–2.89), while high levels of exposure had comparable risk compared to no exposure (RR = 0.94, 95% CI 0.50–1.79). Weak or no associations were observed for other sleep quality outcomes. In stratified analyses participants with mental illness and/or substance use disorder had increased risk ratios for short sleep duration associated with PCE exposure.ConclusionThese findings suggest that early-life exposure to PCE may be associated with a moderate increase in the risk of reporting breathing pauses during sleep in adulthood and that a history of mental illness and/or substance use disorder may exacerbate the risk of short sleep duration.