Polycyclic aromatic hydrocarbon exposure effects on trajectories of maternal and adolescent mental health

Background Parental psychological distress is a well-known risk factor for developmental psychopathology, with longer term parental distress associated with worse youth mental health. Neurotoxicant exposure during pregnancy is a risk factor for both poor maternal and youth mental health. The impact of one class of pollutant, polycyclic aromatic hydrocarbons (PAH), on long-term trajectories of maternal distress and youth self-reported mental health symptoms in adolescence has been understudied. Methods PAH exposure was measured by DNA adducts in maternal blood sampled during the third trimester of pregnancy. Maternal distress, operationalized as maternal demoralization, was measured at 11 timepoints (prenatal to child age 16). Adolescent mental health symptoms were measured at age 13–15. Follow up analyses examined a subset of measures available at age 15–20 years. Structural equation modeling examined associations between PAH exposure during pregnancy and latent growth metrics of maternal distress, and between maternal distress (intercept and slope) and youth mental health symptoms in a prospective longitudinal birth cohort (N = 564 dyads). Results Higher prenatal PAH exposure was associated with higher concurrent maternal distress. Prenatal maternal distress was associated with adolescent’s self-reported anxiety, depression, and externalizing problems. On average, maternal distress declined over time; a slower decline in mother’s distress across the course of the child’s life was associated with greater self-reported anxiety and externalizing problems in youth. Conclusions Our findings are consistent with an intergenerational framework of environmental effects on mental health: PAH exposure during pregnancy affects maternal mental health, which in turn influences mental health outcomes for youth well into adolescence. Future research is necessary to elucidate the possible social and biological mechanisms (e.g., parenting, epigenetics) underlying the intergenerational transmission of the negative effects of pollution on mental health in caregiver-child dyads

Associations of co-exposure to polycyclic aromatic hydrocarbons and lead (Pb) with IGF1 methylation in peripheral blood of preschool children from an e-waste recycling area

BACKGROUND: Childhood exposure to polycyclic aromatic hydrocarbons (PAHs) or lead (Pb) is associated with epigenetic modifications. However, the effects of their co-exposures on IGF1 (Insulin-like growth factor 1) methylation and the potential role in child physical growth are unclear.METHODS: From our previous children study (N = 238, ages of 3-6), 75 children with higher total concentrations of urinary ten hydroxyl PAH metabolites (∑ 10OH-PAHs) from an e-waste recycling area, Guiyu, and 75 with lower ∑ 10OH-PAHs from Haojiang (reference area) were included. Pb and IGF1 P2 promoter methylation in peripheral blood were also measured. Multivariable linear regression analyses were performed to estimate individual associations, overall effects and interactions of co-exposure to OH-PAHs and Pb on IGF1 methylation were further explored using Bayesian kernel machine regression. RESULTS: Methylation of IGF1 (CG-232) was lower (38.00 vs. 39.74 %, P &lt; 0.001), but of CG-207 and CG-137 were higher (59.94 vs. 58.41 %; 57.60 vs. 56.28 %, both P &lt; 0.05) in exposed children than the reference. The elevated urinary 2-OHPhe was associated with reduced methylation of CG-232 (B = -0.051, 95 % CI: -0.096, -0.005, P &lt; 0.05), whereas blood Pb was positively associated with methylation of CG-108 (B = 0.106, 95 %CI: 0.013, 0.199, P &lt; 0.05), even after full adjustment. Methylations of CG-224 and 218 significantly decreased when all OH-PAHs and Pb mixtures were set at 35th - 40th and 45th - 55th percentile compared to when all fixed at 50th percentile. There were bivariate interactions of co-exposure to the mixtures on methylations of CG-232, 224, 218, and 108. Methylations correlated with height, weight, were observed in the exposed children.CONCLUSIONS: Childhood co-exposure to high PAHs and Pb from the e-waste may be associated with IGF1 promoter methylation alterations in peripheral blood. This, in turn, may interrupt the physical growth of preschool children.</p

The Impact of Pollution on Children's Health: A Call for Global Accountability and Enforcement

Environmental pollution in large industrial centers has had a negative impact on the population's health, specifically among children. Our objective is to provide a systematic review of the literature, focusing on the impact of environmental pollutants from urban and metropolitan areas on pediatric health. Disregard for the Earth's atmosphere can negatively impact our fragile ecosystem and create a global toxicity. The impact of industrial growth and economic development has become paramount to modern society. Unfortunately, futuregenerations will pay the consequences of the world's failure to implement regulations to secure a safe environment for our children's health and development. Pollutants penetrate an organism through different routes and change physiological processes, which leads to a decrease in microbial resistance by weakening the child's immune system. The major contaminants are: polycyclic aromatic hydrocarbons, lead, manganese, sulfur dioxide, airborne fine particles, and nitrogen dioxide. Xenobiotics negatively affect the morphological, functional, biochemical parameters, genetics, and epigenetics of the body. It is well documented that the physical development and psychological well-being of children is adversely affected by pollution. The accumulation of heavy metals and other contaminants adversely affected a child's health has been found in the pediatric population. An effort has been made to develop detoxicant remedies, in particular, some enterosorbents and natural adaptogens. Research is ongoing to improve medical rehabilitation of children, who already are affected. Public education and regulations regarding emerging non-pollutant industrial technologies is called for. A global system of accountability and enforcement regarding environmental protection needs to be implemented

Prenatal exposure to fine particles and polycyclic aromatic hydrocarbons and birth outcomes : a two-pollutant approach

Background Previous epidemiologic studies have considered the effects of individual air pollutants on birth outcomes, whereas a multiple-pollutant approach is more relevant to public health policy. Objectives The present study compared the observed effect sizes of prenatal fine particulate matter ( PM2.5) and polycyclic aromatic hydrocarbons (PAH) (a component of PM2.5) exposures on birth outcome deficits, assessed by the single vs. two-pollutant approaches. Methods The study sample included 455 term infants born in Krakow to non-smoking mothers, among whom personal exposures to PM2.5 and PAH were monitored in the second trimester of pregnancy. The exposure effect estimates (unstandardized and standardized regression coefficients) on birth outcomes were determined using evant covariates. Results In the single-pollutant approach, each pollutant was inversely associated with all birth outcomes. The effect size of prenatal PAH exposure on birth weight and length was twice that of PM2.5, in terms of standardized coefficients. In the two-pollutant approach, the negative effect of PM2.5 on birth weight and length, adjusted for PAH exposure, lost its significance. The standardized effect of PAH on birth weight was 10-fold stronger ($\beta$ = -0.20, $\rho$ = 0.004) than that estimated for PM2.5 ($\beta$ = -0.02, $\rho$ = 0.757). Conclusion The results provide evidence that PAH had a greater impact on several measures of fetal development, especially birth weight, than PM2.5. Though in the singlepollutant models PM2.5 had a significant impact on birth outcomes, this effect appears to be mediated by PAH

Effect of Prenatal Exposure to Airborne Polycyclic Aromatic Hydrocarbons on Neurodevelopment in the First 3 Years of Life among Inner-City Children

Our prospective cohort study of nonsmoking African-American and Dominican mothers and children in New York City is evaluating the role of prenatal exposure to urban pollutants, including polycyclic aromatic hydrocarbons (PAHs), environmental tobacco smoke (ETS), and pesticides, in the pathogenesis of neurobehavioral disorders. We used the Bayley Scales of Infant Development to evaluate the effects on child mental and psychomotor development of prenatal exposure to airborne PAHs monitored during pregnancy by personal air sampling. Behavioral development was assessed by the Child Behavior Checklist. We adjusted for potential confounders including sociodemographic factors and prenatal exposure to ETS and chlorpyrifos. Prenatal exposure to PAHs was not associated with psychomotor development index or behavioral problems. However, high prenatal exposure to PAHs (upper quartile) was associated with lower mental development index at age 3 [β= –5.69; 95% confidence interval (CI), –9.05 to –2.33; p < 0.01]. The odds of cognitive developmental delay were also significantly greater for children with high prenatal exposure (odds ratio = 2.89; 95% CI, 1.33 to 6.25; p = 0.01). General estimated equation analysis showed a significant age × PAH effect on mental development (p = 0.01), confirming the age-specific regression findings. Further adjustment for lead did not alter the relationships. There were no differences in effect sizes by ethnicity. The results require confirmation but suggest that environmental PAHs at levels recently encountered in New York City air may adversely affect children’s cognitive development at 3 years of age, with implications for school performance

Using semiparametric‐mixed model and functional linear model to detect vulnerable prenatal window to carcinogenic polycyclic aromatic hydrocarbons on fetal growth

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/106079/1/bimj1458.pd

Chronic Exposure to Low Molecular Weight Polycyclic Aromatic Hydrocarbons Promotes Metabolic Inflammation in Vertebrate and Invertebrate Systems

2-naphthol is a low molecular weight polycyclic aromatic hydrocarbon and ubiquitous air pollutant. Recent epidemiological reports suggest that exposure to individual low molecular weight polycyclic aromatic hydrocarbons is correlated with increased incidences of childhood obesity. Yet, most studies focus on the health effects of either high molecular weight molecules or polycyclic aromatic hydrocarbon mixtures. This research explores the potential obesogenic impact of 2-naphthol in cell and animal models. To assess the in vivo effects of 2-naphthol, we monitored life fitness traits and lipid accumulation in the invertebrate Daphnia magna across development. Results showed that D. magna directly exposed to 2-naphthol demonstrated delayed reproductive development, produced fewer offspring, and accumulated more lipids than D. magna that were not exposed to 2-naphthol. Analysis of lipid accumulation by Nile Red staining revealed a dose-dependent increase in overall lipid quantity. To confirm these findings, we also examined the effect of 2-naphthol on lipid metabolism and inflammation in vitro. We employed 3T3-L1 and BAT1 mammalian cell lines to model white and brown adipocytes, respectively, alongside a murine macrophage cell line (RAW264.7). Cells were challenged with either acute or chronic 2-naphthol treatments, then differentiated adipocytes were assessed for changes in adipogenesis, lipid accumulation, and isoproterenol-stimulated thermogenesis. Additionally, LPS-induced inflammation was evaluated in both adipocytes and macrophages. 2-naphthol exposure increased the expression of key adipogenic and lipogenic genes, while lipolytic gene expression decreased in both chronically treated adipocyte lines. Further, 2-naphthol exposure suppressed isoproterenol-stimulated thermogenic gene expression in BAT1 brown adipocytes. In consistence, adipocytes exposed to 2-naphthol and stained with BODIPY and Oil Red O showed an increase in lipid accumulation. Additionally, adipocytes and macrophages chronically exposed to 2-naphthol showed an up-regulation in mRNA expression of major inflammatory cytokines, such as Tnfα, Il-1β, and Il-6. Overall, these findings support previous research that indicates 2-naphthol is a possible obesogen that may contribute to the development of obesity and associated metabolic disorders via modulating lipid metabolism and thermogenesis in adipocytes, and inflammation in both adipocytes and macrophages

Effects of benzo[a]pyrene and CYP19a1b knockdown on zebrafish development

Benzo[a]pyrene (BaP) is a ubiquitous environmental contaminant that is both an endocrine disruptor and a carcinogen. Aromatase (CYP19) is a key enzyme in steroidogenesis playing a key role in the hypothalamus-pituitary-gonad feedback loop. We hypothesized that BaP would negatively impact cyp19a1b expression in zebrafish, in turn, adversely affecting development and physiology. Here, we consider whether the toxicities observed following BaP exposure are comparable to those following a transient morpholino (MO)-mediated CYP19a1b knockdown or exposure to an aromatase inhibitor (fadrozole) during early development. One-cell zebrafish embryos were injected with a CYP19a1b-MO or control-MO. Other non-injected embryos were exposed to nominal waterborne concentrations of BaP (0, 10 or 50 ?g/L) and fadrozole (0, 10 or 50 ?g/L) for 96 hours post-fertilization (hpf). Real-time PCR shoboth BaP concentrations significantly decreased cyp19a1b expression in 96 hpf zebrafish larvae homogenates. Likewise, concentrations of E2 in 48 hpf whole body larval homogenates were significantly decreased by BaP, fadrozole and CYP19a1b-MO. Cumulative mortality of zebrafish larvae was significantly increased following BaP and fadrozole exposure and CYP19a1b knockdown compared to controls. Estradiol (E2, 10 nM) co-treatment rescued mortality mediated by 10 μg/L BaP, 10 μg/L fadrozole, and CYP19a1b-MO. In a treatment-blinded morphological assessment of larvae at 96 hpf, several phenotypes were negatively impacted by BaP, fadrozole, and CYP19a1b knockdown including body length, optic vesicle size, swim bladder inflation, pericardial and abdominal edema, and incidence of normal larval tail shape and these effects were reversed by exogenous E2-cotreatment. Decreased incidence of normal pectoral fins was only impacted by BaP exposure. In conclusion, certain adverse developmental outcomes caused by BaP exposure are at least in part related to BaP-mediated CYP19a1b inhibition

Seafood Contamination after the BP Gulf Oil Spill and Risks to Vulnerable Populations: A Critique of the FDA Risk Assessment

Background: The BP oil spill of 2010 resulted in contamination of one of the most productive fisheries in the United States by polycyclic aromatic hydrocarbons (PAHs). PAHs, which can accumulate in seafood, are known carcinogens and developmental toxicants. In response to the oil spill, the U.S. Food and Drug Administration (FDA) developed risk criteria and established thresholds for allowable levels [levels of concern (LOCs)] of PAH contaminants in Gulf Coast seafood