Long-term Effects Of Early-life Exposure Research Articles

Sublethal effects of early-life exposure to common and emerging contaminants in birds

The plight of wild birds is becoming critical due to exposure to environmental contaminants. Although laboratory studies have provided insights into the developmental effects of chemical exposures, less is known about the adverse effects of environmental chemicals in developing wild birds. Early life stages are critical windows during which long-term organization of physiological, behavioral, and neurological systems can occur. Thus, contaminant exposure at early life stages can directly influence survival and reproductive success, with consequences for population stability and resilience in wild species. This review synthesizes existing knowledge regarding both short- and long-term effects of early-life exposure to widespread contaminants in birds. We focus especially on wild birds and on contaminants of concern within the Gulf of Mexico as an example of a habitat under anthropogenic stress from exposure to a complex mixture of chemicals and changing land uses that exacerbate existing vulnerabilities of wildlife in this region. Chemical contaminants for discussion in this review are based on avian mortality records from the Wildlife Health Information Sharing Partnership (WHISPers) database and on additional review of the literature regarding avian contaminants of concern for the northern Gulf of Mexico, and include oil and associated polycyclic aromatic hydrocarbons, dioxin and dioxin-like compounds, flame retardants, pesticides, heavy metals, and plastics. We provide an overview of effects in bird species at both the pre-hatching and post-hatching early life stages, discuss differences in sensitivities by route of exposure, life stage, and life history, and provide recommendations for future research. We find that additional research is needed on altricial species, post-hatching early-life exposure, long-term effects, and on ecologically relevant contaminant concentrations and routes of exposure. Given the increasing frequency and intensity of anthropogenic stressors encountered by wild animals, understanding both lethal and sublethal impacts of contaminants on the health of individuals and populations will be critical to inform restoration, management, and mitigation efforts.

Early-life exposure to Saharan dust storms and adolescence functional disability: Evidence from Cameroon

The direct link between early-life dust storm exposure and later-in-life outcomes is not fully understood. This study examines the association of functional disability in a large sample of adolescent Cameroonians (N = 112,855) with in-utero and early childhood exposure to Saharan dust storms. Adjusting all estimations for temperature, precipitation, time and location fixed-effects, and person and family sociodemographic characteristics, we documented adverse effects on functional disability in female adolescents due to exposure to dense dust storms during the third gestation trimester and the second postnatal trimester. We also found suggestive evidence that an effect exists for the first as well as the third through fifth postnatal trimesters. In the third trimester of gestation and the second postnatal trimester, exposure to an average length dust storm with PM10 levels beyond 190 μg/m3 increased the likelihood of disability among female adolescents by approximately 229 (95 % CI: 10–464) in 100,000. The size of the adverse effects for the other periods followed similar patterns.These results show the value of creating infrastructures to mitigate or adapt to the effects of dust storms. These endeavors should focus on communities and populations in and around the Sahara where international organizations can play a role. In addition, establishing health data infrastructures not only improves public health but also advances our understanding of the long-term effects of dust storms. This study demonstrates the importance of research on the long-term effects of early-life exposure to dust storms and the need for additional work on this topic.

Early-life exposure to economic stress and metabolic risks in young adulthood: the children of the reunification in East Germany

BackgroundResearch on the long-term health consequences of early-life exposure to economic crises is scarce. We examine for the first time the long-term effects of early-life exposure to an economic crisis...

Early-life exposure to earthquakes and its long-term effects on human capital outcomes: The case of Myanmar

This paper investigates the long-term effects of early-life exposure to natural disasters on a range of health and educational outcomes, utilizing the spatiotemporal variation in two large earthquakes that occurred in Myanmar in the same year as a natural experiment. The results indicate that cohorts exposed to earthquakes have a higher probability of having at least some difficulty with four activities: seeing, hearing, walking, and remembering. We adopt a battery of alternative specifications and arrive at similar results. Our further results show that earthquakes adversely impact the long-run educational attainment of individuals, exacerbating the pre-existing gender gap in schooling. The findings of this paper provide additional evidence of the importance of timely disaster management as one straightforward way to address the early-life roots of unequal opportunities.

Early-life lead exposure induces long-term toxicity in the central nervous system: From zebrafish larvae to juveniles and adults

Lead induced neurotoxicity has been extensively investigated. However, the potential connections between early-life lead exposure and the frequently observed aberrant neurobehavior in juveniles and adults remain unclear. In this study, zebrafish model was used to explore the immediate and long-term effects of early-life exposure to environmental levels of lead on the central nervous system, and the cellular and molecular mechanisms underlying the consequent abnormal neurobehavior. Lead exposed zebrafish larvae exhibited neurologic damage and defective neurobehavior. Consistent with clinical studies, despite being raised in lead-free conditions, the juvenile and adult fish experienced lead exposure earlier, presented ADHD-like symptoms, and the adult fish exhibited remarkably affected vitality and shoaling behavior. Their anxiety levels were elevated, whereas their social interaction, as well as learning and memory were strongly depressed. The expression profiles of key genes involved in neurodevelopment and neurotransmitter systems were significantly modulated, in similar patterns as in the larval stage. Notably, the density of neurons was decreased and varicosities in neuronal axons were frequently observed in the lead-exposed groups. It's tempting to speculate that the disruption of early neurodevelopment as well as the prolonged modulation of neuromorphic and neurotransmitter systems contribute to the lead-induced neurobehavioral disorders observed in juveniles and adulthood.

Long-term effects of early-life exposure to tropical cyclones

This study evaluates the long-run effects of early-life exposure to tropical cyclones on the socioeconomic performance of individuals in China. We identify significantly negative effects of gestational typhoon exposure on the educational attainment and annual income in adulthood, which also exhibit a significant gender inequality favoring the male. Despite the small culling effects from pregnancy failure and infant mortality, gestational typhoon exposures increase the probability of having a younger sibling and shorten the subsequent birth interval. Typhoon damage to the health and economic abilities of adults, as well as the local economy indicates a channel of household economic status for the reduced long-run socioeconomic outcomes.

Loss of circadian protection against influenza infection in adult mice exposed to hyperoxia as neonates.

Adverse early-life exposures have a lasting negative impact on health. Neonatal hyperoxia that is a risk factor for bronchopulmonary dysplasia confers susceptibility to influenza A virus (IAV) infection later in life. Given our previous findings that the circadian clock protects against IAV, we asked if the long-term impact of neonatal hyperoxia vis-à-vis IAV infection includes circadian disruption. Here, we show that neonatal hyperoxia abolishes the clock-mediated time of day protection from IAV in mice, independent of viral burden through host tolerance pathways. We discovered that the lung intrinsic clock (and not the central or immune clocks) mediated this dysregulation. Loss of circadian protein, Bmal1, in alveolar type 2 (AT2) cells recapitulates the increased mortality, loss of temporal gating, and other key features of hyperoxia-exposed animals. Our data suggest a novel role for the circadian clock in AT2 cells in mediating long-term effects of early-life exposures to the lungs.

The Long-term Effects of Violent Conflict on Women’s Intra-Household Decision-Making Power

Does exposure to civil war during childhood affect women’s later-life intra-household decision-making power? This paper examines the long-term effects of early-life exposure to the Nigerian Civil War on women’s decision-making power within the household, using data from the 2008 Nigerian Demographic and Health Survey. To identify the effects, we adopt a difference-in-differences approach which exploits variation in exposure to the civil war by year of birth and ethnicity. The results show that early-life exposure to the war decreases the likelihood of women’s decision-making power within the household in adulthood. Likely mechanisms include different fertility and marriage choices as well as poorer education, health, and employment outcomes as a result of exposure to the war, which would place women in a more precarious position in the household relative to their partners.

Early-life exposure to 17β-estradiol and 4-nonylphenol impacts the growth hormone/insulin-like growth-factor system and estrogen receptors in Mozambique tilapia, Oreochromis mossambicus

It is widely recognized that endocrine disrupting chemicals (EDCs) released into the environment through anthropogenic activities can have short-term impacts on physiological and behavioral processes and/or sustained or delayed long-term developmental effects on aquatic organisms. While numerous studies have characterized the effects of EDCs on temperate fishes, less is known on the effects of EDCs on the growth and reproductive physiology of tropical species. To determine the long-term effects of early-life exposure to common estrogenic chemicals, we exposed Mozambique tilapia (Oreochromis mossambicus) yolk-sac fry to 17β-estradiol (E2) and nonylphenol (NP) and subsequently characterized the expression of genes involved in growth and reproduction in adults. Fry were exposed to waterborne E2 (0.1 and 1 μg/L) and NP (10 and 100 μg/L) for 21 days. After the exposure period, juveniles were reared for an additional 112 days until males were sampled. Gonadosomatic index was elevated in fish exposed to E2 (0.1 μg/L) while hepatosomatic index was decreased by exposure to NP (100 μg/L). Exposure to E2 (0.1 μg/L) induced hepatic growth hormone receptor (ghr) mRNA expression. The high concentration of E2 (1 μg/L), and both concentrations of NP, increased hepatic insulin-like growth-factor 1 (igf1) expression; E2 and NP did not affect hepatic igf2 and pituitary growth hormone (gh) levels. Both E2 (1 μg/L) and NP (10 μg/L) induced hepatic igf binding protein 1b (igfbp1b) levels while only NP (100 μg/L) induced hepatic igfbp2b levels. By contrast, hepatic igfbp6b was reduced in fish exposed to E2 (1 μg/L). There were no effects of E2 or NP on hepatic igfbp4 and igfbp5a expression. Although the expression of three vitellogenin transcripts was not affected, E2 and NP stimulated hepatic estrogen receptor (erα and erβ) mRNA expression. We conclude that tilapia exposed to E2 and NP as yolk-sac fry exhibit subsequent changes in the endocrine systems that control growth and reproduction during later life stages.

Early-life exposure to the endocrine disruptor 17-α-ethinylestradiol induces delayed effects in adult brain, liver and ovotestis proteomes of a self-fertilizing fish

Early-life represents a critically sensitive window to endocrine disrupting chemicals, potentially leading to long-term repercussions on the phenotype later in life. The mechanisms underlying this phenomenon, referred to as the Developmental Origins of Health and Disease (DOHaD), are still poorly understood. To gain molecular understanding of these effects, we exposed mangrove rivulus (Kryptolebias marmoratus) for 28 days post hatching (dph) to 4 and 120 ng/L 17-α-ethinylestradiol, a model xenoestrogen. After 28 days, fish were raised for 140 days in clean water and we performed quantitative label-free proteomics on brain, liver and ovotestis of 168 dph adults. A total of 820, 888 and 420 proteins were robustly identified in the brain, liver and ovotestis, respectively. Effects of 17-α-ethinylestradiol were tissue and dose-dependent: a total of 31, 51 and 18 proteins were differentially abundant at 4 ng/L in the brain, liver and ovotestis, respectively, compared to 20, 25 and 39 proteins at 120 ng/L. Our results suggest that estrogen-responsive pathways, such as lipid metabolism, inflammation, and the innate immune system were affected months after the exposure. In addition, the potential perturbation of S-adenosylmethionine metabolism encourages future studies to investigate the role of DNA methylation in mediating the long-term effects of early-life exposures. SignificanceThe Developmental Origins of Health and Disease (DOHaD) states that early life stages of humans and animals are sensitive to environmental stressors and can develop health issues later in life, even if the stress has ceased. Molecular mechanisms supporting DOHaD are still unclear. The mangrove rivulus is a new fish model species naturally reproducing by self-fertilization, making it possible to use isogenic lineages in which all individuals are highly homozygous. This species therefore permits to strongly reduce the confounding factor of genetic variability in order to investigate the effects of environmental stress on the phenotype. After characterizing the molecular phenotype of brain, liver and ovotestis, we obtained true proteomic reaction norms of these three organs in adults after early life stages have been exposed to the common endocrine disruptor 17-α-ethinylestradiol (EE2). Our study demonstrates long-term effects of early-life endocrine disruption at the proteomic level in diverse estrogen-responsive pathways 5 months after the exposure. The lowest tested and environmentally relevant concentration of 4 ng/L had the highest impact on the proteome in brain and liver, highlighting the potency of endocrine disruptors at low concentrations.

Selective Mortality and the Long-Term Effects of Early-Life Exposure to Natural Disasters

We analyze the effects of early-life shocks with varying degrees of severity on mortality and human capital outcomes in the Philippines. We exploit variations in typhoon exposure and sharp increases in short-term disaster relief efforts in the 1960s. Severe typhoons are associated with increased mortality and adverse long-term outcomes. Before the increase in disaster relief efforts, mortality from in utero exposure to severe typhoons was 10 percent; survivors exhibited similar levels of human capital as the unaffected. After the increase in disaster relief, the mortality effects were mitigated; however, survivors exhibited lower human capital in the long term.

Marie Vahter: the arsenic detective

Marie Vahter first came across the harm arsenic can do to the environment and health in her native Sweden during the early 1980s, when a large copper smelter was spewing the toxin into the air and sea. She did her PhD in toxicology, focusing her dissertation on the kinetics of inorganic forms of arsenic in relation to animal species. Today, she is a Professor in Environmental Medicine at the Karolinska Institutet, Stockholm, where she directs research into the immediate and long-term effects of early-life exposure to toxic metals such as arsenic, manganese, cadmium, and lead. In Bangladesh, arsenic poisoning is a neglected issueMillions of people in Bangladesh are still being exposed to arsenic in their drinking water, decades after the problem was identified. Sam Loewenberg reports from Dhaka. Full-Text PDF

Long-term effects of early-life exposure to environmental oestrogens on ovarian function: role of epigenetics.

Oestrogens play an important role in development and function of the brain and reproductive tract. Accordingly, it is considered that developmental exposure to environmental oestrogens can disrupt neural and reproductive tract development, potentially resulting in long-term alterations in neurobehaviour and reproductive function. Many chemicals have been shown to have oestrogenic activity, whereas others affect oestrogen production and turnover, resulting in the disruption of oestrogen signalling pathways. However, these mechanisms and the concentrations required to induce these effects cannot account for the myriad adverse effects of environmental toxicants on oestrogen-sensitive target tissues. Hence, alternative mechanisms are assumed to underlie the adverse effects documented in experimental animal models and thus could be important to human health. In this review, the epigenetic regulation of gene expression is explored as a potential target of environmental toxicants including oestrogenic chemicals. We suggest that toxicant-induced changes in epigenetic signatures are important mechanisms underlying the disruption of ovarian follicular development. In addition, we discuss how exposure to environmental oestrogens during early life can alter gene expression through effects on epigenetic control potentially leading to permanent changes in ovarian physiology.

What Do We Know About Short- and Long-Term Effects of Early-Life Exposure to Pollution?

Evidence shows that pollution exposure early in life is detrimental to near-term health, and an increasing body of evidence suggests that early-childhood health influences health and human capital outcomes later in life. This article reviews the economic research that brings these two literatures together. We begin with a conceptual model that highlights the core relationships across the life cycle. We then review the literature concerned with such estimates, focusing particularly on identification strategies to mitigate concerns regarding endogenous exposure. The nascent empirical literature provides both direct and indirect evidence that early-childhood exposure to pollution significantly impacts later-life outcomes. We discuss the potential policy implications of these long-lasting effects and conclude with a number of promising avenues for future research.

Subtle Shades of Impairment: Childhood Tetrachloroethylene Exposure May Cause Subclinical Deficits in Adult Vision

People come into regular contact with tetrachloroethylene (also known as perchloroethylene, or PCE) through dry-cleaned clothes, and the chemical has become a frequent contaminant in surface and groundwater, often due to improper disposal. PCE has been associated with neurologic and visual impairment in exposed adults. Now investigators have detected visual impairment in adults whose exposure to PCE-contaminated drinking water had occurred years earlier—from gestation through age 5 years [EHP 120(9):1327–1332; Getz et al.]. Some 660 miles of improperly cured vinyl-lined drinking water pipes installed between 1968 and 1980 leached PCE into the water delivered to residences at different parts of the Cape Cod region of Massachusetts. Previous studies of this cohort—exposed and unexposed adults born to Cape Cod parents from 1969 through 1983—have detected evidence that PCE exposure may contribute to other neurologic impairments, including post-traumatic stress disorder, bipolar disorder, and diminished performance on tests of memory, learning, and visuospatial functioning. In this study, the investigators tested the visual acuity (sharpness of vision), contrast sensitivity (ability to distinguish gradations of light and dark), and color discrimination (ability to correctly identify colors) in 25 exposed and 40 unexposed members of the cohort. The researchers used an algorithm to estimate PCE exposure based on each individual’s residence during gestation and early childhood, since the presence and degree of PCE contamination in drinking water varied by locale. Tests of color discrimination revealed that high PCE exposure was significantly associated with color confusion, with all major errors occurring in blue–yellow discrimination. Only the highest PCE exposure level was associated with impaired contrast sensitivity, but these results were not statistically significant. Visual acuity did not appear to be affected; most study participants had 20:20 vision, and no differences were observed between exposure groups. The measured vision impairments are subclinical, meaning they would not have directly noticeable effects on an individual’s vision. Previous studies have only assessed relationships between PCE exposure and vision in either childhood or adulthood. The results of this retrospective study must be confirmed, given its small sample size, but the findings suggest that childhood PCE exposure may cause long-term visual impairment. Further study of this or other exposed populations is necessary to understand the long-term effects of early-life exposure to PCE.