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MicroRNAs as Potential Signatures of Environmental Exposure or Effect: A Systematic Review

Karen Vrijens, Valentina Bollati, Tim S. Nawrot

Environmental Health Perspectives · 2015 · Systematic review · Public domain

doi:10.1289/ehp.1408459

Abstract

Background: The exposome encompasses all life-course environmental exposures from the prenatal period onward that influence health. MicroRNAs (miRNAs) are interesting entities within this concept as markers and causation of disease. MicroRNAs are short oligonucleotide sequences that can interact with several mRNA targets. Objectives: We reviewed the current state of the field on the potential of using miRNAs as biomarkers for environmental exposure. We investigated miRNA signatures in response to all types of environmental exposure to which a human can be exposed, including cigarette smoke, air pollution, nanoparticles, and diverse chemicals; and we examined the health conditions for which the identified miRNAs have been reported (i.e., cardiovascular disease, cancer, and diabetes). Methods: We searched the PubMed and ScienceDirect databases to identify relevant studies. Results: For all exposures incorporated in this review, 27 miRNAs were differentially expressed in at least two independent studies. miRNAs that had expression alterations associated with smoking observed in multiple studies are miR-21, miR-34b, miR-125b, miR-146a, miR-223, and miR-340; and those miRNAs that were observed in multiple air pollution studies are miR-9, miR-10b, miR-21, miR-128, miR-143, miR-155, miR-222, miR-223, and miR-338. We found little overlap among in vitro, in vivo, and human studies between miRNAs and exposure. Here, we report on disease associations for those miRNAs identified in multiple studies on exposure. Conclusions: miRNA changes may be sensitive indicators of the effects of acute and chronic environmental exposure. Therefore, miRNAs are valuable novel biomarkers for exposure. Further studies should elucidate the role of the mediation effect of miRNA between exposures and effect through all stages of life to provide a more accurate assessment of the consequences of miRNA changes. Citation: Vrijens K, Bollati V, Nawrot TS. 2015. MicroRNAs as potential signatures of environmental exposure or effect: a systematic review. Environ Health Perspect 123:399–411; http://dx.doi.org/10.1289/ehp.1408459

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 18, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

Most common diseases result from the combined effect of genes and environmental factors and the interactions between them. Epigenetic effects and non-coding gene products have gained research focus over the last two decades because protein-coding genes cannot account for all observed genomic effects. Here we focus on microRNAs (miRNAs) as key regulators of health and disease. miRNAs are endogenous, single-stranded, short non-coding RNA sequences (~ 22 nucleotides) that regulate gene expression at the posttranscriptional level. Since the first discovery of miRNAs in Caenorhabditis elegans, hundreds of miRNAs in eukaryotes have been identified to influence physiological processes such as development, growth, differentiation, immune reaction, and adaptation to stress. Diverse disease states, such as cancer and heart failure, are associated with distinct miRNA signatures, suggesting that specific miRNA programs are activated in pathophysiological processes.

Recent advances in molecular biology opened the opportunity for new approaches in population-based studies, in which exposures to a broad spectrum of environmental pollutants are evaluated in concert with biological systems, a concept proposed as the “exposome”. From this viewpoint, miRNAs could potentially be novel biomarkers of exposure. For the purpose of this review, we focused on the response of miRNAs to environmental exposures.

miRNA characteristics. miRNA-mediated gene silencing is accomplished by base pairing of the 5´ region of miRNAs with the target mRNA sequence, leading to translational repression and/or mRNA degradation. miRNAs have been paradoxically shown to up-regulate gene expression by enhancing translation under specific conditions. The effect of miRNA expression on gene expression is not linear, as multiple miRNAs may target the same mRNA, and the majority of mRNAs contain multiple binding sites for miRNAs, generating a highly complex regulatory network system. For details on miRNA synthesis, biogenesis, miRNA mechanism of action, see Figure 1 and reviews by and.

miRNA nomenclature. miRNAs are named using the “miR” prefix and a unique identifying number (e.g., miR-1, miR-2). The identifying numbers are assigned sequentially, with identical miRNAs having the same number, regardless of organism. Paralogous sequences whose mature miRNAs differ at only one or two positions are given lettered suffixes: for example, miR-10a and miR-10b. Distinct hairpin loci that give rise to identical mature miRNAs have numbered suffixes (e.g., mir-281-1, mir-281-2). The mature sequences are designated “miR,” whereas the precursor hairpins are labeled “mir.” The -3p and -5p suffixes that sometimes appear within an miR name refer to the arm from which the mature sequence comes. For nomenclature guidelines, see.

miRNA analysis techniques suitable for large epidemiological studies. In recent years, miRNA expression changes following exposure to environmental toxicants, even before disease onset, have gained researchers’ interest. The measure of miRNAs in large epidemiological studies needs to be high throughput and sensitive enough to detect small changes in healthy subjects. At the same time, techniques need to be affordable in order to be conducted in large population studies. Moreover, given the complexity of phenomena induced by exposure but not fully explained by an effect on a single transcript, current research is going toward genome-wide techniques. Another challenge is tissue specificity of miRNAs: The availability of only noninvasive samples in epidemiological studies conducted on healthy populations limits our capability to investigate target tissues and opens important questions on the meaning of those markers in surrogate tissues. In epidemiological research, free and exosomal miRNAs in body fluids are interesting study objects because of their potential to serve as a proxy for tissue-specific miRNAs. A limitation of this approach is that these miRNAs differ between different body fluids, and their function is not clear. Although miRNAs hold promise as exposure biomarkers, recent studies have been primarily disease focused [reviewed by ].

Genome-wide miRNA analysis can be achieved by amplification-based [real-time quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR)], hybridization-based (microarrays), and sequencing-based [next-generation sequencing (NGS)] technologies. Method selection depends on the type of sample to be analyzed and the RNA preparation protocol used. qRT-PCR is considered the gold standard because of its sensitivity, specificity, accuracy, and simple protocols. qRT-PCR can evaluate candidate miRNA expression or array plates that include a large number of miRNAs in one reaction, to OpenArray® (Applied Biosystems, Life Technologies), which allows the simultaneous amplification of a very large panel of miRNAs using nanoscale volumes. In a recent review, compared qRT-PCR to different array-based platforms used to study mRNAs/miRNAs.

Several miRNA microarray chip platforms that are commercially available [e.g., Affymetrix GeneChip® 3.0 miRNA array (Affymetrix Inc.), Agilent Human miRNA Microarray system (Agilent Technologies), Exiqon miRCURY LNA™ microarray (Exiqon Inc.)] differ in probe design and detection stringency. The limitation of this microarray chip method is the availability and stringency of probes on the chip platform that pair with miRNAs of interest. Microarrays have the advantage of being easily correlated to mRNA expression data, thus providing functional information. Furthermore, unlike other current miRNA analysis techniques, microarrays allow fast analysis of miRNAs without an arbitrary preselection step. However, the large amount of data produced can generate false-positive results, and the time-consuming step of validation by qRT-PCR is almost necessary.

NGS strategies based on deep sequencing overcome some of the technical drawbacks of probe-based methodologies, especially the ability to detect only previously known sequences. As miRNAs are sequenced directly, information about sequence variations or posttranscriptional RNA editing becomes available for further analysis. The newly developed Nanostring nCounter 27 (Nanostring Technologies Inc.) uses two sequence-specific capture probes to allow for discrimination between similar variants of a single miRNA. NGS technologies [e.g., Illumina/Solexa (Illumina Inc.), GA Roche/454 GS FLX Titanium (Roche Diagnostics Corp.), and ABI/SOLID (Applied Biosystems)] allow complete “miRnomes” to be sequenced and allow for the discovery of novel miRNAs and isoforms. Another benefit of NGS technology is that it can identify precursor and primary miRNAs as well as their mature forms. NGS will likely become the gold standard for miRNA analysis because of its ability to sequence short fragments in a high-throughput mode. The choice between these methods is a key factor in establishing the possibility of success of any epidemiological study. Each method has pros and cons and should be evaluated based on the specific research.

Methods

Search strategy and selection criteria. To identify the articles relevant to this topic, we undertook a comprehensive search of the PubMed (http://www.ncbi.nlm.nih.gov/pubmed) and ScienceDirect (http://www.sciencedirect.com/) databases initially using “microRNA” and “environmental exposure” as key terms. We did additional searches in which we replaced “microRNA” with “mir,” “miRNA,” or “epigenetic changes” and we substituted “environmental exposure” with “smoking,” “passive smoking,” “cigarette smoke,” “air pollution,” “nanoparticle exposure,” “bisphenol A,” “endocrine disruptors,” or “chemical exposure” in every possible combination. We also considered review articles as well as references found in our literature search. We excluded articles not written in English. The PubMed search covered 1 January 1980 to 1 June 2014. Articles dealing only with the description of single nucleotide polymorphisms (SNPs) in miRNA genes were disregarded, as were those articles dealing only with the description of miRNAs in nonmammalian species. A flowchart detailing the search strategy is presented in Figure 2. For miRNAs differentially expressed in response to more than one personal or environmental exposure, we researched disease phenotypes correlated with them by searching each of these miRNAs on the Human microRNA Disease Database (HMDD; http://202.38.126.151/hmdd/mirna/md/) and the miR2Disease Base (http://www.mir2disease.org/). Results of these searches are presented in Table 1, including the direction of regulation (up or down) of the miRNA and the ensuing phenotype.

Results

Smoking-induced changes in miRNA expression. The most studied environmental factor in relation to epigenetics is smoking; it was among the first factors shown to affect the miRNA machinery in humans. Results of in vitro studies concerning smoking and miRNAs are summarized in Table 2.

analyzed miRNA expression patterns in the lungs of mice exposed to passive cigarette smoke, and they established life-course–related miRNA expression changes by comparing miRNA expression in lungs from unexposed newborn, postweaning, and adult mice. These researchers observed developmental-stage–specific miRNA expression profiles in which miRNAs that were highly expressed in newborns tended to be less expressed in adult mice and vice versa, whereas miRNA expression in postweaning mice was intermediate. Results from in vivo studies concerning smoking and miRNAs are shown in Table 3.

Two studies reported a comparison between mRNA and miRNA whole genome expression patterns for smokers and nonsmokers. reported that quitting smoking altered the plasma miRNA profiles to resemble those of nonsmokers. In addition, Let-7c and miR-150 could be of importance in the initiation of smoke-induced decline of lung function, because genes that were associated with lung function impairment in genome-wide association studies have been reported to be significantly enriched in binding sites for these miRNAs, namely STAT3 and TNFR-II.

The effect of in utero exposures on health during childhood and later in life is a growing area of research interest with major public health implications. An adaptive response in the fetus to in utero exposures can result in persistent changes into adulthood. miRNA expression levels in placenta can affect health later in life. Studies on miRNA expression and human exposure at different stages of life (in utero, adult) are included in Table 4.

Not surprisingly, miRNAs that are frequently observed to be down-regulated in response to smoking have also been identified as down-regulated in lung, pancreatic, and stomach cancer. Development of cardiovascular disease is associated with up-regulation of miR-206, and this miRNA has significantly higher expression levels in smokers than in nonsmokers. Furthermore, two miRNAs that are frequently down-regulated in association with cigarette smoke (i.e., miR-21 and miR-146a) have lower expression levels in individuals with type 2 diabetes compared with healthy controls. Therefore, these miRNAs could support the observation that smoking is an independent risk factor for type 2 diabetes. Human studies concerning smoking-induced changes of miRNA expression are summarized in Table 4. Figure 3 is a Venn diagram displaying the common and distinct miRNAs from in vitro, in vivo, and human studies on smoking-induced miRNA alterations. miR-125b and miR-21, identified in in vivo and human studies, respectively, were also reported in in vitro studies. Furthermore, several miRNAs were identified in multiple studies, such as miR-34b and miR-146a.

Table 1 summarizes miRNAs with altered expression in response to environmental and/or personal exposures reported in at least two independent studies, along with their known roles in disease etiology. miRNAs observed in association with either environmental or personal exposures are often associated with cancer; in particular, breast and lung cancer and leukemia have been frequently reported (Table 1). Furthermore, many aberrations in the cardiovascular system have been reported, such as hypertension, heart failure, myocardial infarct, and atherosclerosis. Exposures such as air pollution and smoking can cause cardiovascular disease and cancer; however, the data shown in Table 1 indicate that the listed miRNAs play a causative role in disease etiology, rather than being merely a marker of exposure.

Air pollution exposure and miRNA expression. Particulate matter (PM) is a complex mixture of small particles and liquid droplets. Particle pollution is made up of a number of components, including acids, organic chemicals, metals, and soil or dust particles. The size of particles is directly linked to their potential to cause health problems. Although the clinical effects of PM exposure are obvious, the underlying mechanism of disease initiation and progression is less well understood. miRNAs play a pivotal role in maintaining healthy lungs. Because the lungs are an important target site for PM, we suggest that miRNAs could underlie the observed health effects of PM exposure. In vitro studies on air pollution and miRNAs are summarized in Table 5.

In a cohort study of steel plant workers, examined the effect of PM exposure on miRNA expression. Blood samples were collected at the beginning of the working week (“preexposure”) and at the end of the working week (“postexposure”). PM mass and metal components measured in the plant were correlated with miRNA expression analyses of blood samples. Urinary 8-hydroxy-2´-deoxyguanosine (8-OH-dG) levels were measured as a readout of oxidative stress. Both miR-222 and miR-21 were significantly increased in post- versus preexposure samples, and only miR-21 expression levels were positively correlated with 8-OH-dG. Oxidative stress has been reported to induce miR-21 expression; thus, the association between 8-OH-dG and miR-21 might simply reflect the response of miR-21 to production of reactive oxygen species (ROS) in the blood due to the PM-induced increase in oxidative stress (Table 6).

The cardiovascular anomalies observed in association with air pollution exposure have often been attributed to the generation of oxidative stress. MiR-21 is up-regulated in response to diesel exhaust particles and metal-rich PM and is highly expressed in the cardiovascular system, where it plays an important role in vascular cell proliferation and apoptosis and disease [reviewed by ]. Therefore, miR-21 expression could be an important mechanistic link explaining the association between air pollution exposure and cardiovascular disease.

observed distinct miRNA expression profiles in patients with asthma compared with controls after subway exposure. Current epidemiological studies have identified the first miRNAs associated with air pollution exposure, and provide a list of putative biomarkers. Table 6 summarizes the human studies on air pollution and miRNAs. A Venn diagram displays the common and distinct miRNAs from in vitro and human studies on air pollution–induced miRNA alterations (Figure 4). The only miRNAs identified in both in vitro and human studies in association with air pollution exposure are miR-10b and miR-128. Furthermore, miRNAs -9, -21, -143, -155, -222, -223, and -338 were identified in at least two independent studies on air pollution and miRNA.

Nanoparticles. Nanoparticles are emitted from natural and anthropogenic sources and are produced via nanotechnology. Fast propagation of nanotechnologies into different industries and consumer products is causing exponential growth of nanomaterial production. Hence, increasing amounts of nanoparticles reach occupational settings and the indoor and outdoor environments, thus representing a potentially serious hazard to human health. Nanoparticles are also able to cross cell membranes, and their interactions with biological systems are relatively unknown. Table 7 includes the studies on nanoparticle-induced changes in miRNA expression, all of which were performed in animal models.

Chemical exposure-induced changes in miRNA. Formaldehyde. Formaldehyde is an air toxic present in the atmosphere due to emission from anthropogenic and biogenic sources. Ninety-five percent of inhaled formaldehyde is absorbed within the respiratory tract. Formaldehyde has been reported to change gene expression patterns in nasal and lung cells. The miRNAs reported to be down-regulated in association with formaldehyde exposure have been reported to be involved in the development of diverse tumors (e.g., breast and gastrointestinal cancer, melanoma) as well as heart failure (Table 1). Given the capability of formaldehyde to pass deep into lung tissue and enter systemic circulation, the link with cardiovascular disease and cancer has been widely discussed [reviewed by ]. Interestingly, miR-181a, one of the miRNAs down-regulated after formaldehyde exposure, was reported to affect the DNA damage response in breast cancer, enabling the identification of aggressive breast tumors based on increased miR-181a expression.

Endocrine disruptors. Organochlorine pesticides and plasticizing agents are ubiquitous environmental endocrine-disrupting compounds that impact human health. Bisphenol A (BPA) is an industrial plasticizer often used as a coating in food cans and in plastic bottles. Dichlorodiphenyltrichloroethane (DDT) is a well-known organochlorine pesticide. Because DDT is very persistent in the environment, accumulates in fatty tissues, and can travel long distances in the upper atmosphere, residues from historical use remain a current threat to human health.

DDT and BPA have been reported to interfere with endogenous estrogens and thyroid hormone, leading to aberrations of the reproductive, immune, and central nervous systems. DDT and BPA cross the placental barrier and can induce in utero effects that could lead to detrimental effects later in life.

reported that prenatal exposure to BPA can alter mammary development and lead to breast cancer in humans. From a clinical perspective, it is interesting that decreased expression of let-7f has been associated with increased breast cancer risk, and treatment of MCF-7 breast cancer cells with BPA resulted in reduced let-7f expression. Furthermore, miR-146a has been proposed to induce an Alzheimer’s disease pathway and is up-regulated after BPA exposure (Table 1). Therefore, the neurodegenerative consequences of BPA exposure could at least partially be attributed to miR-146a. In vitro studies could provide researchers with interesting miRNAs that have potential to be used as biomarkers for chemical exposure.

Polychlorinated biphenyls (PCBs) were widely used organic chemicals until their production was banned because of environmental concerns. PCBs are stable compounds that bioaccumulate in fatty tissues; they have been reported to cause systemic changes in gene expression, suggesting that miRNA regulation could be involved in this process. reported an association between maternal PCB exposure and fetal toxicity, impaired fetal growth, and pregnancy loss.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been reported to adversely affect the immune system in rats. In addition, reported that TCDD exposure of pregnant mice affected the immune system of fetuses by suppressing T-cell function. Given the regulatory role miRNAs play in the immune system, it can be expected that miRNAs are important in regulating the detrimental health effects observed after exposure to TCDD and PCBs.

Arsenic. Environmental exposure to arsenic, especially to trivalent inorganic arsenic (As3+), is a health concern given the high concentrations present in groundwater across the world. Exposure to arsenic has been associated with increased risk of cancer due to genomic instability, and long-term arsenic exposure has been observed to induce peripheral vascular injury. A Venn diagram showing the common and distinct miRNAs from in vitro and human studies on arsenic-induced miRNA alterations is presented in Figure 5. Only miRNA-21 was associated with arsenic exposure in in vitro model systems and in human studies. Three miRNAs were identified by at least two independent studies on arsenic exposure and miRNA expression, namely, miR-26b, miR-181a, and miR-222.

Aluminum sulfates. Aluminum is the most widely distributed metal in the environment and is extensively used in daily life. Chronic exposure of animals to aluminum is associated with behavioral and neuropathological changes. Epidemiological studies have shown poor performance in cognitive tests and a higher abundance of neurological symptoms in workers occupationally exposed to aluminum.

Hexahydro-1,3,5-trinitro-s-triazine (RDX). The polynitramine explosive RDX is a heavily used second-generation high explosive, and its use can result in the contamination of soils, sediments, and water. RDX exposure has been reported to be toxic to the neural and immune systems and to increase tumor incidence in several cancers.

Diethylstilbestrol (DES). The synthetic estrogen DES was prescribed to pregnant women from the 1940s to the 1960s in order to prevent miscarriages; however, DES was later reported to be responsible for increasing breast cancer in the mothers and gynecologic tumor incidence in their exposed daughters.

Perfluorooctanoic acid (PFOA). Perfluoroalkyl chemicals (PFCs) are highly stable and widely used in industrialized countries. PFCs are both lipophobic and hydrophobic; thus, after absorption they will bind to proteins in serum and liver rather than accumulate in lipids. PFOA is one of the most commonly used PFCs.

The studies we reviewed on chemical-induced changes in miRNA expression are summarized in Tables 8–10 by type of study: in vitro (Table 8), in vivo (Table 9), and human (Table 10) studies.

Conclusions

miRNAs are omnipresent in the genome and are important regulators of gene expression in response to intracellular as well as environmental cues. In this review, we examined the response of the miRNA machinery to personal and environmental exposures, including air pollution, cigarette smoking, and chemicals such as endocrine disruptors. miRNAs have been proposed as biomarkers for disease; however, the literature also reveals their potential to be used as biomarkers of environmental exposure.

In different studies on the same environmental pollutant, overall the identified miRNAs showed similar patterns of expression regulation. In studies where smoking-induced changes were investigated, the general observation was a down-regulation of expression. For example, miR-125b was down-regulated in response to cigarette smoke in both primary human bronchial epithelial cells and mouse lung tissue. However, when unique miRNAs had altered expression patterns in response to different environmental exposures, their direction of regulation could be the same (10/25 miRNAs) or the opposite (15/25 miRNAs; 60%). The different exposures we discussed here have their own unique health effects, so one would not expect them to have the same effect on the miRNA machinery. However, there is sometimes a discrepancy when looking at the same exposure indicator; for example, in response to smoking, miR-21 has been reported to be up-regulated in some studies and down-regulated in others (Table 4). Part of the discrepancy can be explained by the different exposure models that were used.

In general, different in vitro studies show little overlap, potentially because of the complex miRNA–mRNA networks that underlie the observations and the differences in exposure used across studies. In studies of the same environmental pollutant in vitro, in vivo, or in humans, identified miRNAs were quite distinct (Figures 3–5). This can be explained in part by the observation that animal models do not always reflect genomic responses that occur in humans. Discrepancy between different studies might also stem from differences in exposure duration. For example, in a study in rats, the duration of exposure uniquely influenced expression patterns of the individual miRNAs.

Human epidemiological studies are necessary to observe exposure-related effects on miRNAs. Understanding the exposome requires putting together pieces of a complex puzzle. Epidemiological studies need input from experimental studies to identify good candidate biomarkers, and results from epidemiological studies often need follow-up by experimental studies to investigate mechanisms of action and to study tissue dependency of effects because human studies are most often performed in easily accessible tissues such as blood and saliva as a surrogate for the actual target tissues.

Currently, epidemiological studies on microRNA often involve free or exosomal miRNAs present in saliva or other body fluids. However, it is not clear whether these observed miRNA changes are a true reflection of the body’s response and can really predict health effects. In blood, miRNAs within the exosomes have been shown to overlap with cellular miRNA profiles: observed that exosomes derived from blood were enriched for miRNAs and that miRNA profiles between blood cells and the cell-free exosomal fraction showed important overlap.

Because miRNAs can regulate mRNA expression in both a negative manner and a positive manner and because many miRNAs can bind the same mRNA, it is difficult to draw conclusions from miRNA studies without infomation on the concurrent mRNA(s) expression pattern. However, this information is rare in current reports on epidemiological studies of miRNAs. The findings of this review underscore the complex networks that are built by miRNAs and the mRNAs they regulate because one miRNA can influence many mRNAs according to the timing and pattern of expression.

Many of the reviewed studies used large-scale microarray profiling, but follow-up and validation with more quantitative approaches often lags behind. This delay is understandable because of the cost and labor intensity inherent to these techniques; however, it is important to confirm the miRNAs that are responsive to environmental exposures.

Researchers are currently publishing extensive lists of miRNAs that are responsive to environmental exposures and showing their utility as biomarkers of effect. Future research should focus on identifying the molecular mechanism behind miRNA expression changes in response to exposure to determine whether the changes in miRNA expression are merely a symptom of the (patho)physiological processes the organism undergoes after exposure, or whether miRNAs are the drivers responsible for these changes. recently reviewed the putative mechanisms of action behind miRNAs’ response to environmental exposure. However, the effect of the identified miRNAs on putative mRNA targets should also be studied to determine whether the change in miRNA expression has functional consequences and which mRNAs are true miRNA targets under the given circumstances.

At present, little is known about whether environmental exposures induce long-term changes in human miRNA expression or whether these have a transient character. To address this problem, more longitudinal studies should be conducted to examine the long-term effects of exposure. Results from animal studies suggest that miRNA expression changes in response to formaldehyde exposure are transient and revert to normal levels after recovery from exposure, but reported that miRNA profiles in target organs did not recover 1 week after cessation of long-term cigarette smoke exposure. In a study in humans, observed that miRNA expression profiles of individuals who quit smoking resembled those of nonsmokers.

Follow-up in future generations is necessary to determine the heritability of the miRNA expression changes. It would be very interesting to examine the effect of in utero environmental exposures on development of disease in later life and the role miRNAs play in inducing these health effects. Furthermore, long-term longitudinal studies would allow us to distinguish between cause and effect of miRNA expression and environmental exposure, and would also allow us to estimate the contribution of miRNAs to disease development. Studies have shown that miRNAs can be used as biomarkers of disease as well as biomarkers for environmental exposure and that miRNAs hold great potential to explain disease etiology.

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    Not in our library10.1038/leu.2011.356

  27. 27.

    Dai Y, Sui W, Lan H, Yan Q, Huang H, Huang Y. Comprehensive analysis of microRNA expression patterns in renal biopsies of lupus nephritis patients. Rheumatol Int. 2009;29(7):749-754.

    Not in our library10.1007/s00296-008-0758-6

  28. 28.

    Davis JL, Wani AH, O’Neal BR, Hansen LD. RDX biodegradation column study: comparison of electron donors for biologically induced reductive transformation in groundwater. J Hazard Mater. 2004;112(1–2):45-54.

    Not in our library10.1016/j.jhazmat.2004.03.020

  29. 29.

    Deng Q Huang S Zhang X Zhang W Feng J Wang T 2014 Plasma microRNA expression and micronuclei frequency in workers exposed to polycyclic aromatic hydrocarbons.Environ Health Perspect122719725;

    Not in our library10.1289/ehp.1307080

  30. 30.

    D’hulst AI, Bracke KR, Maes T, De Bleecker JL, Pauwels RA, Joos GF, et al. Role of tumour necrosis factor-α receptor P75 in cigarette smoke–induced pulmonary inflammation and emphysema. Eur Respir J. 2006;28:102-112.

    Not in our library10.1183/09031936.06.00059305

  31. 31.

    Djuranovic S, Nahvi A, Green R. A parsimonious model for gene regulation by miRNAs. Science. 2011;331(6017):550-553.

    Not in our library10.1126/science.1191138

  32. 32.

    Dulout FN, Grillo CA, Seoane AI, Maderna CR, Nilsson R, Vahter M, et al. Chromosomal aberrations in peripheral blood lymphocytes from native Andean women and children from northwestern Argentina exposed to arsenic in drinking water. Mutat Res. 1996;370(3–4):151-158.

    Not in our library10.1016/s0165-1218(96)00060-2

  33. 33.

    Earle JS, Luthra R, Romans A, Abraham R, Ensor J, Yao H, et al. Association of microRNA expression with microsatellite instability status in colorectal adenocarcinoma. J Mol Diagn. 2010;12(4):433-440.

    Not in our library10.2353/jmoldx.2010.090154

  34. 34.

    Etheridge A, Lee I, Hood L, Galas D, Wang K. Extracellular microRNA: a new source of biomarkers. Mutat Res. 2011;717(1–2):85-90.

    Not in our library10.1016/j.mrfmmm.2011.03.004

  35. 35.

    Eyholzer M, Schmid S, Schardt JA, Haefliger S, Mueller BU, Pabst T. Complexity of miR-223 regulation by CEBPA in human AML. Leuk Res. 2010;34(5):672-676.

    Not in our library10.1016/j.leukres.2009.11.019

  36. 36.

    Faith RE, Luster MI. Investigations on the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on parameters of various immune functions. Ann NY Acad Sci. 1979;320:564-571.

    Not in our library10.1111/j.1749-6632.1979.tb56634.x

  37. 37.

    Feitelson MA, Lee J. Hepatitis B virus integration, fragile sites, and hepatocarcinogenesis. Cancer Lett. 2007;252(2):157-170.

    Not in our library10.1016/j.canlet.2006.11.010

  38. 38.

    Fendorf S, Michael HA, van Geen A. Spatial and temporal variations of groundwater arsenic in South and Southeast Asia. Science. 2010;328(5982):1123-1127.

    Not in our library10.1126/science.1172974

  39. 39.

    Ferretti E, De Smaele E, Po A, Di Marcotullio L, Tosi E, Espinola MS, et al. MicroRNA profiling in human medulloblastoma. Int J Cancer. 2009;124(3):568-577.

    Not in our library10.1002/ijc.23948

  40. 40.

    Fossati S, Baccarelli A, Zanobetti A, Hoxha M, Vokonas PS, Wright RO, et al. Ambient particulate air pollution and microRNAs in elderly men. Epidemiology. 2014;25(1):68-78.

    Not in our library10.1097/ede.0000000000000026

  41. 41.

    Fry RC, Rager JE, Bauer R, Sebastian E, Peden DB, Jaspers I, et al. Air toxics and epigenetic effects: ozone altered microRNAs in the sputum of human subjects. Am J Physiol Lung Cell Mol Physiol. 2014;306(12):L1129-L1137.

    Not in our library10.1152/ajplung.00348.2013

  42. 42.

    Fulgenzi A Vietti D Ferrero ME 2014 Aluminium involvement in neurotoxicity.Biomed Res Int758323;

    Not in our library10.1155/2014/758323

  43. 43.
    Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients · 2010
    Not checked
  44. 44.
    Plasma levels of lipometabolism-related miR-122 and miR-370 are increased in patients with hyperlipidemia and associated with coronary artery disease · 2012
    No notice
  45. 45.

    Gao W, Yu Y, Cao H, Shen H, Li X, Pan S, et al. Deregulated expression of miR-21, miR-143 and miR-181a in non small cell lung cancer is related to clinicopathologic characteristics or patient prognosis. Biomed Pharmacother. 2010;64(6):399-408.

    Not in our library10.1016/j.biopha.2010.01.018

  46. 46.

    Garcia-Reyero N, Habib T, Pirooznia M, Gust KA, Gong P, Warner C, et al. Conserved toxic responses across divergent phylogenetic lineages: a meta-analysis of the neurotoxic effects of RDX among multiple species using toxicogenomics. Ecotoxicology. 2011;20(3):580-594.

    Not in our library10.1007/s10646-011-0623-3

  47. 47.

    Genovesi LA Carter KW Gottardo NG Giles KM Dallas PB 2011 Integrated analysis of miRNA and mRNA expression in childhood medulloblastoma compared with neural stem cells.PloS one69e23935;

    Not in our library10.1371/journal.pone.0023935

  48. 48.

    Gluckman PD, Hanson MA, Cooper C, Thornburg KL. Effect of in utero and early-life conditions on adult health and disease. N Engl J Med. 2008;359(1):61-73.

    Not in our library10.1056/nejmra0708473

  49. 49.

    Graff JW Powers LS Dickson AM Kim J Reisetter AC Hassan IH 2012 Cigarette smoking decreases global microRNA expression in human alveolar macrophages.PloS One78e44066;

    Not in our library10.1371/journal.pone.0044066

  50. 50.

    Greco S, Fasanaro P, Castelvecchio S, D’Alessandra Y, Arcelli D, Di Donato M, et al. MicroRNA dysregulation in diabetic ischemic heart failure patients. Diabetes. 2012;61(6):1633-1641.

    Not in our library10.2337/db11-0952

  51. 51.

    Greenberg ER, Barnes AB, Resseguie L, Barrett JA, Burnside S, Lanza LL, et al. Breast cancer in mothers given diethylstilbestrol in pregnancy. N Engl J Med. 1984;311(22):1393-1398.

    Not in our library10.1056/nejm198411293112201

  52. 52.

    Guida M, Marra M, Zullo F, Guida M, Trifuoggi M, Biffali E, et al. Association between exposure to dioxin-like polychlorinated biphenyls and miR-191 expression in human peripheral blood mononuclear cells. Mutat Res. 2013;753(1):36-41.

    Not in our library10.1016/j.mrgentox.2012.12.018

  53. 53.

    Halappanavar S, Nikota J, Wu D, Williams A, Yauk CL, Stampfli M. IL-1 receptor regulates microRNA-135b expression in a negative feedback mechanism during cigarette smoke-induced inflammation. J Immunol. 2013;190(7):3679-3686.

    Not in our library10.4049/jimmunol.1202456

  54. 54.

    Henke JI, Goergen D, Zheng J, Song Y, Schüttler CG, Fehr C, et al. microRNA-122 stimulates translation of hepatitis C virus RNA. EMBO J. 2008;27(24):3300-3310.

    Not in our library10.1038/emboj.2008.244

  55. 55.

    Herberth G, Bauer M, Gasch M, Hinz D, Röder S, Olek S, et al. Maternal and cord blood miR-223 expression associates with prenatal tobacco smoke exposure and low regulatory T-cell numbers. J Allergy Clin Immunol. 2013;133(2):543-550.

    Not in our library10.1016/j.jaci.2013.06.036

  56. 56.

    Holsapple MP, Farland WH, Landry TD, Monteiro-Riviere NA, Carter JM, Walker NJ, et al. Research strategies for safety evaluation of nanomaterials, part II: toxicological and safety evaluation of nanomaterials, current challenges and data needs. Toxicol Sci. 2005;88(1):12-17.

    Not in our library10.1093/toxsci/kfi293

  57. 57.

    Hu Y, Li P, Hao S, Liu L, Zhao J, Hou Y. Differential expression of microRNAs in the placentae of Chinese patients with severe pre-eclampsia. Clin Chem Lab Med. 2009;47(8):923-929.

    Not in our library10.1515/cclm.2009.228

  58. 58.

    Huang Y, Dai Y, Zhang J, Wang C, Li D, Cheng J, et al. Circulating microRNAs as potential biomarkers for smoking-related interstitial fibrosis. Biomarkers. 2012;17(5):435-440.

    Not in our library10.3109/1354750x.2012.680611

  59. 59.

    Hulsmans M, Sinnaeve P, Van der Schueren B, Mathieu C, Janssens S, Holvoet P. Decreased miR-181a expression in monocytes of obese patients is associated with the occurrence of metabolic syndrome and coronary artery disease. J Clin Endocrinol Metab. 2012;97(7):E1213-E1218.

    Not in our library10.1210/jc.2012-1008

  60. 60.

    Izzotti A, Calin GA, Steele VE, Croce CM, De Flora S. Relationships of microRNA expression in mouse lung with age and exposure to cigarette smoke and light. FASEB J. 2009;23(9):3243-3250.

    Not in our library10.1096/fj.09-135251

  61. 61.

    Izzotti A, Larghero P, Longobardi M, Cartiglia C, Camoirano A, Steele VE, et al. Dose-responsiveness and persistence of microRNA expression alterations induced by cigarette smoke in mouse lung. Mutat Res. 2011;717(1–2):9-16.

    Not in our library10.1016/j.mrfmmm.2010.12.008

  62. 62.

    Izzotti A, Pulliero A. The effects of environmental chemical carcinogens on the microRNA machinery. Int J Hyg Environ Health. 2014;217(6):601-627.

    Not in our library10.1016/j.ijheh.2014.01.001

  63. 63.
    Disruption of MicroRNA Expression in Human Airway Cells by Diesel Exhaust Particles Is Linked to Tumorigenesis-Associated Pathways · 2009
    No notice
  64. 64.

    Ji R, Cheng Y, Yue J, Yang J, Liu X, Chen H, et al. MicroRNA expression signature and antisense-mediated depletion reveal an essential role of MicroRNA in vascular neointimal lesion formation. Circ Res. 2007;100(11):1579-1588.

    Not in our library10.1161/circresaha.106.141986

  65. 65.

    Jiang W, Zhang Y, Meng F, Lian B, Chen X, Yu X, et al. Identification of active transcription factor and miRNA regulatory pathways in Alzheimer’s disease. Bioinformatics. 2013;29(20):2596-2602.

    Not in our library10.1093/bioinformatics/btt423

  66. 66.

    Jin L, Hu WL, Jiang CC, Wang JX, Han CC, Chu P, et al. MicroRNA-149*, a p53-responsive microRNA, functions as an oncogenic regulator in human melanoma. Proc Natl Acad Sci USA. 2011;108(38):15840-15845.

    Not in our library10.1073/pnas.1019312108

  67. 67.

    Ju X, Li D, Shi Q, Hou H, Sun N, Shen B. Differential microRNA expression in childhood B-cell precursor acute lymphoblastic leukemia. Pediatr Hematol Oncol. 2009;26(1):1-10.

    Not in our library10.1080/08880010802378338

  68. 68.

    Kang JH, Kondo F, Katayama Y. Human exposure to bisphenol A. Toxicology. 2006;226(2–3):79-89.

    Not in our library10.1016/j.tox.2006.06.009

  69. 69.

    Kim K, Lee HC, Park JL, Kim M, Kim SY, Noh SM, et al. Epigenetic regulation of microRNA-10b and targeting of oncogenic MAPRE1 in gastric cancer. Epigenetics. 2011;6(6):740-751.

    Not in our library10.4161/epi.6.6.15874

  70. 70.

    Kim KH, Jahan SA, Kabir E. A review of diseases associated with household air pollution due to the use of biomass fuels. J Hazard Mater. 2011;192(2):425-431.

    Not in our library10.1016/j.jhazmat.2011.05.087

  71. 71.

    Kim WJ, Terada N, Nomura T, Takahashi R, Lee SD, Park JH, et al. Effect of formaldehyde on the expression of adhesion molecules in nasal microvascular endothelial cells: the role of formaldehyde in the pathogenesis of sick building syndrome. Clin Exp Allergy. 2002;32(2):287-295.

    Not in our library10.1046/j.1365-2222.2002.01301.x

  72. 72.
    Tissue‐ and Plasma‐Specific MicroRNA Signatures for Atherosclerotic Abdominal Aortic Aneurysm · 2012
    No notice
  73. 73.

    Kong AP, Xiao K, Choi KC, Wang G, Chan MH, Ho CS, et al. Associations between microRNA (miR-21, 126, 155 and 221), albuminuria and heavy metals in Hong Kong Chinese adolescents. Clin Chim Acta. 2012;413(13–14):1053-1057.

    Not in our library10.1016/j.cca.2012.02.014

  74. 74.

    Kong W, He L, Richards EJ, Challa S, Xu CX, Permuth-Wey J, et al. Upregulation of miRNA-155 promotes tumour angiogenesis by targeting VHL and is associated with poor prognosis and triple-negative breast cancer. Oncogene. 2014;33(6):679-689.

    Not in our library10.1038/onc.2012.636

  75. 75.

    Kumar V, Gill KD. Aluminium neurotoxicity: neurobehavioural and oxidative aspects. Arch Toxicol. 2009;83(11):965-978.

    Not in our library10.1007/s00204-009-0455-6

  76. 76.

    Lau P, de Strooper B. Dysregulated microRNAs in neurodegenerative disorders. Semin Cell Dev Biol. 2010;21(7):768-773.

    Not in our library10.1016/j.semcdb.2010.01.009

  77. 77.

    Lee RC, Feinbaum RL, Ambros V. The C. elegans heterochronic gene lin-4 encodes small RNAs with antisense complementarity to lin-14. Cell. 1993;75(5):843-854.

    Not in our library10.1016/0092-8674(93)90529-y

  78. 78.

    Leucci E, Zriwil A, Gregersen LH, Jensen KT, Obad S, Bellan C, et al. Inhibition of miR-9 de-represses HuR and DICER1 and impairs Hodgkin lymphoma tumour outgrowth in vivo. Oncogene. 2012;31(49):5081-5089.

    Not in our library10.1038/onc.2012.15

  79. 79.

    Levänen B, Bhakta NR, Torregrosa Paredes P, Barbeau R, Hiltbrunner S, Pollack JL, et al. Altered microRNA profiles in bronchoalveolar lavage fluid exosomes in asthmatic patients. J Allergy Clin Immunol. 2013;131(3):894-903.

    Not in our library10.1016/j.jaci.2012.11.039

  80. 80.

    Li GY Lee HY Shin HS Kim HY Lim CH Lee BH 2007 Identification of gene markers for formaldehyde exposure in humans.Environ Health Perspect11514601466;

    Not in our library10.1289/ehp.10180

  81. 81.

    Li X, Liu Y, Song G, Liu N. A microarray for microRNA profiling in spermatozoa from adult men living in an environmentally polluted site. Bull Environ Contam Toxicol. 2012a;89(6):1111-1114.

    Not in our library10.1007/s00128-012-0827-0

  82. 82.

    Li X, Shi Y, Wei Y, Ma X, Li Y, Li R. Altered expression profiles of microRNAs upon arsenic exposure of human umbilical vein endothelial cells. Environ Toxicol Pharmacol. 2012b;34(2):381-387.

    Not in our library10.1016/j.etap.2012.05.003

  83. 83.

    Liang P, Lv C, Jiang B, Long X, Zhang P, Zhang M, et al. MicroRNA profiling in denatured dermis of deep burn patients. Burns. 2012;38(4):534-540.

    Not in our library10.1016/j.burns.2011.10.014

  84. 84.

    Liu C Duan W Li R Xu S Zhang L Chen C 2013 Exposure to bisphenol A disrupts meiotic progression during spermatogenesis in adult rats through estrogen-like activity.Cell Death Dis4e676;

    Not in our library10.1038/cddis.2013.203

  85. 85.

    Liu XX, Li XJ, Zhang B, Liang YJ, Zhou CX, Cao DX, et al. MicroRNA-26b is underexpressed in human breast cancer and induces cell apoptosis by targeting SLC7A11. FEBS Lett. 2011;585(9):1363-1367.

    Not in our library10.1016/j.febslet.2011.04.018

  86. 86.

    Lukiw WJ, Alexandrov PN. Regulation of complement factor H (CFH) by multiple miRNAs in Alzheimer’s disease (AD) brain. Mol Neurobiol. 2012;46(1):11-19.

    Not in our library10.1007/s12035-012-8234-4

  87. 87.

    Lukiw WJ, Dua P, Pogue AI, Eicken C, Hill JM. Upregulation of micro RNA-146a (miRNA-146a), a marker for inflammatory neurodegeneration, in sporadic Creutzfeldt-Jakob disease (sCJD) and Gerstmann-Straussler-Scheinker (GSS) syndrome. J Toxicol Environ Health A. 2011;74(22–24):1460-1468.

    Not in our library10.1080/15287394.2011.618973

  88. 88.

    Lukiw WJ, Pogue AI. Induction of specific micro RNA (miRNA) species by ROS-generating metal sulfates in primary human brain cells. J Inorg Biochem. 2007;101(9):1265-1269.

    Not in our library10.1016/j.jinorgbio.2007.06.004

  89. 89.

    Lv SQ, Kim YH, Giulio F, Shalaby T, Nobusawa S, Yang H, et al. Genetic alterations in microRNAs in medulloblastomas. Brain Pathol. 2012;22(2):230-239.

    Not in our library10.1111/j.1750-3639.2011.00523.x

  90. 90.

    Ma L, Young J, Prabhala, Pan E, Mestdagh P, Muth D, et al. miR-9, a MYC/MYCN-activated microRNA, regulates E-cadherin and cancer metastasis. Nat Cell Biol. 2010;12(3):247-256.

    Not in our library10.1038/ncb2024

  91. 91.

    Maccani MA, Avissar-Whiting M, Banister CE, McGonnigal B, Padbury JF, Marsit CJ. Maternal cigarette smoking during pregnancy is associated with downregulation of miR-16, miR-21, and miR-146a in the placenta. Epigenetics. 2010;5(7):583-589.

    Not in our library10.4161/epi.5.7.12762

  92. 92.
    miR-16 and miR-21 Expression in the Placenta Is Associated with Fetal Growth · 2011
    No notice
  93. 93.

    Marcucci G, Radmacher MD, Maharry K, Mrózek K, Ruppert AS, Paschka P, et al. MicroRNA expression in cytogenetically normal acute myeloid leukemia. N Engl J Med. 2008;358(18):1919-1928.

    Not in our library10.1056/nejmoa074256

  94. 94.

    Marczylo EL, Amoako AA, Konje JC, Gant TW, Marczylo TH. Smoking induces differential miRNA expression in human spermatozoa: a potential transgenerational epigenetic concern? Epigenetics. 2012;7(5):432-439.

    Not in our library10.4161/epi.19794

  95. 95.

    Miller MR, Shaw CA, Langrish JP. From particles to patients: oxidative stress and the cardiovascular effects of air pollution. Future Cardiol. 2012;8(4):577-602.

    Not in our library10.2217/fca.12.43

  96. 96.

    Miller TE, Ghoshal K, Ramaswamy B, Roy S, Datta J, Shapiro CL, et al. MicroRNA-221/222 confers tamoxifen resistance in breast cancer by targeting p27Kip1. J Biol Chem. 2008;283(44):29897-29903.

    Not in our library10.1074/jbc.m804612200

  97. 97.

    Mittendorf R. Teratogen update: carcinogenesis and teratogenesis associated with exposure to diethylstilbestrol (DES) in utero. Teratology. 1995;51(6):435-445.

    Not in our library10.1002/tera.1420510609

  98. 98.

    Motta V, Angelici L, Nordio F, Bollati V, Fossati S, Frascati F, et al. Integrative analysis of miRNA and inflammatory gene expression after acute particulate matter exposure. Toxicol Sci. 2013;132(2):307-316.

    Not in our library10.1093/toxsci/kft013

  99. 99.

    Murchison EP, Hannon GJ. miRNAs on the move: miRNA biogenesis and the RNAi machinery. Curr Opin Cell Biol. 2004;16(3):223-229.

    Not in our library10.1016/j.ceb.2004.04.003

  100. 100.

    Nagano T Higashisaka K Kunieda A Iwahara Y Tanaka K Nagano K 2013 Liver-specific microRNAs as biomarkers of nanomaterial-induced liver damage.Nanotechnology2440405102;

    Not in our library10.1088/0957-4484/24/40/405102

  101. 101.

    Nagel R, le Sage C, Diosdado B, van der Waal M, Oude Vrielink JA, Bolijn A, et al. Regulation of the adenomatous polyposis coli gene by the miR-135 family in colorectal cancer. Cancer Res. 2008;68(14):5795-5802.

    Not in our library10.1158/0008-5472.can-08-0951

  102. 102.

    Nakanishi H, Taccioli C, Palatini J, Fernandez-Cymering C, Cui R, Kim T, et al. Loss of miR-125b-1 contributes to head and neck cancer development by dysregulating TACSTD2 and MAPK pathway. Oncogene. 2014;33(6):702-712.

    Not in our library10.1038/onc.2013.13

  103. 103.

    Nana-Sinkam SP, Hunter MG, Nuovo GJ, Schmittgen TD, Gelinas R, Galas D, et al. Integrating the microRNome into the study of lung disease. Am J Respir Crit Care Med. 2009;179(1):4-10.

    Not in our library10.1164/rccm.200807-1042pp

  104. 104.

    Nel A, Xia T, Mädler L, Li N. Toxic potential of materials at the nanolevel. Science. 2006;311(5761):622-627.

    Not in our library10.1126/science.1114397

  105. 105.

    Ohlsson Teague EM, Van der Hoek KH, Van der Hoek MB, Perry N, Wagaarachchi P, Robertson SA, et al. MicroRNA-regulated pathways associated with endometriosis. Mol Endocrinol. 2009;23(2):265-275.

    Not in our library10.1210/me.2008-0387

  106. 106.

    Ota D, Mimori K, Yokobori T, Iwatsuki M, Kataoka A, Masuda N, et al. Identification of recurrence-related microRNAs in the bone marrow of breast cancer patients. Int J Oncol. 2011;38(4):955-962.

    Not in our library10.3892/ijo.2011.926

  107. 107.

    Overton JH, Kimbell JS, Miller FJ. Dosimetry modeling of inhaled formaldehyde: the human respiratory tract. Toxicol Sci. 2001;64(1):122-134.

    Not in our library10.1093/toxsci/64.1.122

  108. 108.

    Pallante P, Visone R, Ferracin M, Ferraro A, Berlingieri MT, Troncone G, et al. MicroRNA deregulation in human thyroid papillary carcinomas. Endocr Relat Cancer. 2006;13(2):497-508.

    Not in our library10.1677/erc.1.01209

  109. 109.

    Palma CA Al Sheikha D Lim TK Bryant A Vu TT Jayaswal V 2014 MicroRNA-155 as an inducer of apoptosis and cell differentiation in Acute Myeloid Leukaemia.Mol Cancer13179;

    Not in our library10.1186/1476-4598-13-79

  110. 110.
    microRNA expression in the prefrontal cortex of individuals with schizophrenia and schizoaffective disorder · 2007
    No notice
  111. 111.

    Pogue AI, Li YY, Cui JG, Zhao Y, Kruck TP, Percy ME, et al. Characterization of an NF-κB-regulated, miRNA-146a-mediated down-regulation of complement factor H (CFH) in metal-sulfate-stressed human brain cells. J Inorg Biochem. 2009;103(11):1591-1595.

    Not in our library10.1016/j.jinorgbio.2009.05.012

  112. 112.

    Polikepahad S, Knight JM, Naghavi AO, Oplt T, Creighton CJ, Shaw C, et al. Proinflammatory role for let-7 microRNAS in experimental asthma. J Biol Chem. 2010;285(39):30139-30149.

    Not in our library10.1074/jbc.m110.145698

  113. 113.
    Lung Cancer and Cardiovascular Disease Mortality Associated with Ambient Air Pollution and Cigarette Smoke: Shape of the Exposure–Response Relationships · 2011
    No notice
  114. 114.

    Porta M, Zumeta E. Implementing the Stockholm Treaty on Persistent Organic Pollutants [Editorial]. Occup Environ Med. 2002;59(10):651-652.

    Not in our library10.1136/oem.59.10.651

  115. 115.

    Prokopec SD, Watson JD, Waggott DM, Smith AB, Wu AH, Okey AB, et al. Systematic evaluation of medium-throughput mRNA abundance platforms. RNA. 2013;19(1):51-62.

    Not in our library10.1261/rna.034710.112

  116. 116.

    Qian ZR, Asa SL, Siomi H, Siomi MC, Yoshimoto K, Yamada S, et al. Overexpression of HMGA2 relates to reduction of the let-7 and its relationship to clinicopathological features in pituitary adenomas. Mod Pathol. 2009;22(3):431-441.

    Not in our library10.1038/modpathol.2008.202

  117. 117.

    Qu P, Roberts J, Li Y, Albrecht M, Cummings OW, Eble JN, et al. Stat3 downstream genes serve as biomarkers in human lung carcinomas and chronic obstructive pulmonary disease. Lung Cancer. 2009;63:341-347.

    Not in our library10.1016/j.lungcan.2008.05.025

  118. 118.

    Rager JE Moeller BC Doyle-Eisele M Kracko D Swenberg JA Fry RC 2013 Formaldehyde and epigenetic alterations: microRNA changes in the nasal epithelium of nonhuman primates.Environ Health Perspect121339344;

    Not in our library10.1289/ehp.1205582

  119. 119.

    Rager JE, Moeller BC, Miller SK, Kracko D, Doyle-Eisele M, Swenberg JA, et al. Formaldehyde-associated changes in microRNAs: tissue and temporal specificity in the rat nose, white blood cells, and bone marrow. Toxicol Sci. 2014;138(1):36-46.

    Not in our library10.1093/toxsci/kft267

  120. 120.

    Rager JE Smeester L Jaspers I Sexton KG Fry RC 2011 Epigenetic changes induced by air toxics: formaldehyde exposure alters miRNA expression profiles in human lung cells.Environ Health Perspect119494500;

    Not in our library10.1289/ehp.1002614

  121. 121.

    Rahman MM, Qian ZR, Wang EL, Sultana R, Kudo E, Nakasono M, et al. Frequent overexpression of HMGA1 and 2 in gastroenteropancreatic neuroendocrine tumours and its relationship to let-7 downregulation. Br J Cancer. 2009;100(3):501-510.

    Not in our library10.1038/sj.bjc.6604883

  122. 122.

    Raitoharju E, Lyytikäinen LP, Levula M, Oksala N, Mennander A, Tarkka M, et al. miR-21, miR-210, miR-34a, and miR-146a/b are up-regulated in human atherosclerotic plaques in the Tampere Vascular Study. Atherosclerosis. 2011;219(1):211-217.

    Not in our library10.1016/j.atherosclerosis.2011.07.020

  123. 123.

    Ralfkiaer U, Hagedorn PH, Bangsgaard N, Løvendorf MB, Ahler CB, Svensson L, et al. Diagnostic microRNA profiling in cutaneous T-cell lymphoma (CTCL). Blood. 2011;118(22):5891-5900.

    Not in our library10.1182/blood-2011-06-358382

  124. 124.

    Rubin BS. Bisphenol A: an endocrine disruptor with widespread exposure and multiple effects. J Steroid Biochem Mol Biol. 2011;127(1–2):27-34.

    Not in our library10.1016/j.jsbmb.2011.05.002

  125. 125.

    Saetrom P, Heale BS, Snøve O, Aagaard L, Alluin J, Rossi JJ. Distance constraints between microRNA target sites dictate efficacy and cooperativity. Nucleic Acids Res. 2007;35:2333-2342.

    Not in our library10.1093/nar/gkm133

  126. 126.

    Sakurai M, Miki Y, Masuda M, Hata S, Shibahara Y, Hirakawa H, et al. LIN28: a regulator of tumor-suppressing activity of let-7 microRNA in human breast cancer. J Steroid Biochem Mol Biol. 2012;131(3–5):101-106.

    Not in our library10.1016/j.jsbmb.2011.10.007

  127. 127.

    Scapoli L, Palmieri A, Lo Muzio L, Pezzetti F, Rubini C, Girardi A, et al. MicroRNA expression profiling of oral carcinoma identifies new markers of tumor progression. Int J Immunopathol Pharmacol. 2010;23(4):1229-1234.

    Not in our library10.1177/039463201002300427

  128. 128.

    Schembri F, Sridhar S, Perdomo C, Gustafson AM, Zhang X, Ergun A, et al. MicroRNAs as modulators of smoking-induced gene expression changes in human airway epithelium. Proc Natl Acad Sci USA. 2009;106(7):2319-2324.

    Not in our library10.1073/pnas.0806383106

  129. 129.

    Schulte JH, Marschall T, Martin M, Rosenstiel P, Mestdagh P, Schlierf S, et al. Deep sequencing reveals differential expression of microRNAs in favorable versus unfavorable neuroblastoma. Nucleic Acids Res. 2010;38(17):5919-5928.

    Not in our library10.1093/nar/gkq342

  130. 130.

    Seok J, Warren HS, Cuenca AG, Mindrinos MN, Baker HV, Xu W, et al. Genomic responses in mouse models poorly mimic human inflammatory diseases. Proc Natl Acad Sci USA. 2013;110(9):3507-3512.

    Not in our library10.1073/pnas.1222878110

  131. 131.

    Shan ZX, Lin QX, Fu YH, Deng CY, Zhou ZL, Zhu JN, et al. Upregulated expression of miR-1/miR-206 in a rat model of myocardial infarction. Biochem Biophys Res Commun. 2009;381(4):597-601.

    Not in our library10.1016/j.bbrc.2009.02.097

  132. 132.

    Shi L, Cheng Z, Zhang J, Li R, Zhao P, Fu Z, et al. hsa-mir-181a and hsa-mir-181b function as tumor suppressors in human glioma cells. Brain Res. 2008;1236:185-193.

    Not in our library10.1016/j.brainres.2008.07.085

  133. 133.
    Prenatal exposure to TCDD triggers significant modulation of microRNA expression profile in the thymus that affects consequent gene expression. · 2012
    Not checked
  134. 134.

    Song MK, Park YK, Ryu JC. Polycyclic aromatic hydrocarbon (PAH)-mediated upregulation of hepatic microRNA-181 family promotes cancer cell migration by targeting MAPK phosphatase-5, regulating the activation of p38 MAPK. Toxicol Appl Pharmacol. 2013;273(1):130-139.

    Not in our library10.1016/j.taap.2013.08.016

  135. 135.

    Soto AM, Brisken C, Schaeberle C, Sonnenschein C. Does cancer start in the womb? Altered mammary gland development and predisposition to breast cancer due to in utero exposure to endocrine disruptors. J Mammary Gland Biol Neoplasia. 2013;18(2):199-208.

    Not in our library10.1007/s10911-013-9293-5

  136. 136.

    Spira A, Beane J, Shah V, Liu G, Schembri F, Yang X, et al. Effects of cigarette smoke on the human airway epithelial cell transcriptome. Proc Natl Acad Sci USA. 2004;101(27):10143-10148.

    Not in our library10.1073/pnas.0401422101

  137. 137.

    Stánitz E, Juhász K, Tóth C, Gombos K, Natali PG, Ember I. Evaluation of MicroRNA expression pattern of gastric adenocarcinoma associated with socioeconomic, environmental and lifestyle factors in northwestern Hungary. Anticancer Res. 2013;33(8):3195-3200.

    Not in our library

  138. 138.

    Steele G, Stehr-Green P, Welty E. Estimates of the biologic half-life of polychlorinated biphenyls in human serum [Letter]. N Engl J Med. 1986;314(14):926-927.

    Not in our library10.1056/nejm198604033141418

  139. 139.

    Sturchio E, Colombo T, Boccia P, Carucci N, Meconi C, Minoia C, et al. Arsenic exposure triggers a shift in microRNA expression. Sci Total Environ. 2014;472:672-680.

    Not in our library10.1016/j.scitotenv.2013.11.092

  140. 140.

    Sweeney LM, Okolica MR, Gut CP, Gargas ML. Cancer mode of action, weight of evidence, and proposed cancer reference value for hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX). Regul Toxicol Pharmacol. 2012;64(2):205-224.

    Not in our library10.1016/j.yrtph.2012.07.005

  141. 141.

    Takahashi K, Yokota S, Tatsumi N, Fukami T, Yokoi T, Nakajima M. Cigarette smoking substantially alters plasma microRNA profiles in healthy subjects. Toxicol Appl Pharmacol. 2013;272(1):154-160.

    Not in our library10.1016/j.taap.2013.05.018

  142. 142.
    Disposition of orally administered 2,2-Bis(4-hydroxyphenyl)propane (Bisphenol A) in pregnant rats and the placental transfer to fetuses. · 2000
    No notice
  143. 143.

    Takamizawa J, Konishi H, Yanagisawa K, Tomida S, Osada H, Endoh H, et al. Reduced expression of the let-7 microRNAs in human lung cancers in association with shortened postoperative survival. Cancer Res. 2004;64(11):3753-3756.

    Not in our library10.1158/0008-5472.can-04-0637

  144. 144.

    Thum T, Galuppo P, Wolf C, Fiedler J, Kneitz S, van Laake LW, et al. MicroRNAs in the human heart: a clue to fetal gene reprogramming in heart failure. Circulation. 2007;116(3):258-267.

    Not in our library10.1161/circulationaha.107.687947

  145. 145.
    Endocrine Disruptor Regulation of MicroRNA Expression in Breast Carcinoma Cells · 2012
    No notice
  146. 146.

    Tseng CH. Cardiovascular disease in arsenic-exposed subjects living in the arseniasis-hyperendemic areas in Taiwan. Atherosclerosis. 2008;199(1):12-18.

    Not in our library10.1016/j.atherosclerosis.2008.02.013

  147. 147.

    Tsukimori K Tokunaga S Shibata S Uchi H Nakayama D Ishimaru T 2008 Long-term effects of polychlorinated biphenyls and dioxins on pregnancy outcomes in women affected by the Yusho incident.Environ Health Perspect116626630;

    Not in our library10.1289/ehp.10686

  148. 148.

    Van Pottelberge GR, Mestdagh P, Bracke KR, Thas O, van Durme YM, Joos GF, et al. MicroRNA expression in induced sputum of smokers and patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2011;183(7):898-906.

    Not in our library10.1164/rccm.201002-0304oc

  149. 149.

    van Rooij E, Sutherland LB, Qi X, Richardson JA, Hill J, Olson EN. Control of stress-dependent cardiac growth and gene expression by a microRNA. Science. 2007;316(5824):575-579.

    Not in our library10.1126/science.1139089

  150. 150.

    Vasudevan S, Tong Y, Steitz JA. Switching from repression to activation: microRNAs can up-regulate translation. Science. 2007;318(5858):1931-1934.

    Not in our library10.1126/science.1149460

  151. 151.

    Voellenkle C, van Rooij J, Cappuzzello C, Greco S, Arcelli D, Di Vito L, et al. MicroRNA signatures in peripheral blood mononuclear cells of chronic heart failure patients. Physiol Genomics. 2010;42(3):420-426.

    Not in our library10.1152/physiolgenomics.00211.2009

  152. 152.

    Vogt M, Munding J, Grüner M, Liffers ST, Verdoodt B, Hauk J, et al. Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. Virchows Arch. 2011;458(3):313-322.

    Not in our library10.1007/s00428-010-1030-5

  153. 153.

    Volinia S, Calin GA, Liu CG, Ambs S, Cimmino A, Petrocca F, et al. A microRNA expression signature of human solid tumors defines cancer gene targets. Proc Natl Acad Sci USA. 2006;103(7):2257-2261.

    Not in our library10.1073/pnas.0510565103

  154. 154.

    Waliszewski SM, Aguirre AA, Infanzon RM, Silva CS, Siliceo J. Organochlorine pesticide levels in maternal adipose tissue, maternal blood serum, umbilical blood serum, and milk from inhabitants of Veracruz, Mexico. Arch Environ Contam Toxicol. 2001;40(3):432-438.

    Not in our library10.1007/s002440010194

  155. 155.

    Wang C, Yang C, Chen X, Yao B, Yang C, Zhu C, et al. Altered profile of seminal plasma microRNAs in the molecular diagnosis of male infertility. Clin Chem. 2011;57(12):1722-1731.

    Not in our library10.1373/clinchem.2011.169714

  156. 156.

    Wang F Liu W Jin Y Wang F Ma J 2014 Prenatal and neonatal exposure to perfluorooctane sulfonic acid results in aberrant changes in miRNA expression profile and levels in developing rat livers.Environ Toxicol; [Online 13 January 2014]

    Not in our library10.1002/tox.21949

  157. 157.
    Serum MicroRNA Signatures Identified by Solexa Sequencing Predict Sepsis Patients’ Mortality: A Prospective Observational Study · 2012
    No notice
  158. 158.

    Wang J, Zhang Y, Zhang W, Jin Y, Dai J. Association of perfluorooctanoic acid with HDL cholesterol and circulating miR-26b and miR-199-3p in workers of a fluorochemical plant and nearby residents. Environ Sci Technol. 2012;46(17):9274-9281.

    Not in our library10.1021/es300906q

  159. 159.

    Wang X, Ha T, Liu L, Zou J, Zhang X, Kalbfleisch J, et al. Increased expression of microRNA-146a decreases myocardial ischaemia/reperfusion injury. Cardiovasc Res. 2013;97(3):432-442.

    Not in our library10.1093/cvr/cvs356

  160. 160.

    Wang Y, Li Z, He C, Wang D, Yuan X, Chen J, et al. MicroRNAs expression signatures are associated with lineage and survival in acute leukemias. Blood Cells Mol Dis. 2010;44(3):191-197.

    Not in our library10.1016/j.bcmd.2009.12.010

  161. 161.

    Weigelt K, Bergink V, Burgerhout KM, Pescatori M, Wijkhuijs A, Drexhage HA. Down-regulation of inflammation-protective microRNAs 146a and 212 in monocytes of patients with postpartum psychosis. Brain Behav Immun. 2013;29:147-155.

    Not in our library10.1016/j.bbi.2012.12.018

  162. 162.

    White NM, Bao TT, Grigull J, Youssef YM, Girgis A, Diamandis M, et al. miRNA profiling for clear cell renal cell carcinoma: biomarker discovery and identification of potential controls and consequences of miRNA dysregulation. J Urol. 2011;186(3):1077-1083.

    Not in our library10.1016/j.juro.2011.04.110

  163. 163.

    Wild C. Complementing the genome with an “exposome”: the outstanding challenge of environmental exposure measurement in molecular epidemiology. Cancer Epidemiol Biomarkers Prev. 2005;14(8):1847-1850.

    Not in our library10.1158/1055-9965.epi-05-0456

  164. 164.

    Williams AH, Valdez G, Moresi V, Qi X, McAnally J, Elliott JL, et al. MicroRNA-206 delays ALS progression and promotes regeneration of neuromuscular synapses in mice. Science. 2009;326(5959):1549-1554.

    Not in our library10.1126/science.1181046

  165. 165.

    Wong KY, Liang R, So CC, Jin DY, Costello JF, Chim CS. Epigenetic silencing of MIR203 in multiple myeloma. Br J Haematol. 2011;154(5):569-578.

    Not in our library10.1111/j.1365-2141.2011.08782.x

  166. 166.

    Wu J, Yang T, Li X, Yang Q, Liu R, Huang J, et al. Alteration of serum miR-206 and miR-133b is associated with lung carcinogenesis induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. Toxicol Appl Pharmacol. 2013;267(3):238-246.

    Not in our library10.1016/j.taap.2013.01.002

  167. 167.

    Wu ZS, Wu Q, Wang CQ, Wang XN, Huang J, Zhao JJ, et al. miR-340 inhibition of breast cancer cell migration and invasion through targeting of oncoprotein c-Met. Cancer. 2011;117(13):2842-2852.

    Not in our library10.1002/cncr.25860

  168. 168.

    Xi S Yang M Tao Y Xu H Shan J Inchauste S 2010 Cigarette smoke induces C/EBP-β-mediated activation of miR-31 in normal human respiratory epithelia and lung cancer cells.PLoS One510e13764;

    Not in our library10.1371/journal.pone.0013764

  169. 169.

    Xiao C, Calado DP, Galler G, Thai TH, Patterson HC, Wang J, et al. MiR-150 controls B cell differentiation by targeting the transcription factor c-Myb. Cell. 2007;131(1):146-159.

    Not in our library10.1016/j.cell.2007.07.021

  170. 170.

    Xu CC, Han WQ, Xiao B, Li NN, Zhu DL, Gao PJ. Differential expression of microRNAs in the aorta of spontaneously hypertensive rats [in Chinese]. Sheng Li Xue Bao. 2008;60(4):553-560.

    Not in our library

  171. 171.

    Yamagishi M, Nakano K, Miyake A, Yamochi T, Kagami Y, Tsutsumi A, et al. Polycomb-mediated loss of miR-31 activates NIK-dependent NF-κB pathway in adult T cell leukemia and other cancers. Cancer Cell. 2012;21(1):121-135.

    Not in our library10.1016/j.ccr.2011.12.015

  172. 172.

    Yamamoto M Singh A Sava F Pui M Tebbutt SJ Carlsten C 2013 MicroRNA expression in response to controlled exposure to diesel exhaust: attenuation by the antioxidant N-acetylcysteine in a randomized crossover study.Environ Health Perspect121670675;

    Not in our library10.1289/ehp.1205963

  173. 173.

    Yanaihara N, Caplen N, Bowman E, Seike M, Kumamoto K, Yi M, et al. Unique microRNA molecular profiles in lung cancer diagnosis and prognosis. Cancer cell. 2006;9(3):189-198.

    Not in our library10.1016/j.ccr.2006.01.025

  174. 174.

    Yi C, Wang Q, Wang L, Huang Y, Li L, Liu L, et al. MiR-663, a microRNA targeting p21(WAF1/CIP1), promotes the proliferation and tumorigenesis of nasopharyngeal carcinoma. Oncogene. 2012;31(41):4421-4433.

    Not in our library10.1038/onc.2011.629

  175. 175.

    Yuchuan H, Ya D, Jie Z, Jingqiu C, Yanrong L, Dongliang L, et al. Circulating miRNAs might be promising biomarkers to reflect the dynamic pathological changes in smoking-related interstitial fibrosis. Toxicol Ind Health. 2014;30(2):182-191.

    Not in our library10.1177/0748233712452606

  176. 176.

    Zampetaki A, Kiechl S, Drozdov I, Willeit P, Mayr U, Prokopi M, et al. Plasma microRNA profiling reveals loss of endothelial miR-126 and other microRNAs in type 2 diabetes. Circ Res. 2010;107(6):810-817.

    Not in our library10.1161/circresaha.110.226357

  177. 177.

    Zhang B Pan X 2009 RDX induces aberrant expression of microRNAs in mouse brain and liver.Environ Health Perspect117231240;

    Not in our library10.1289/ehp.11841

  178. 178.

    Zhang JX, Song W, Chen ZH, Wei JH, Liao YJ, Lei J, et al. Prognostic and predictive value of a microRNA signature in stage II colon cancer: a microRNA expression analysis. Lancet Oncol. 2013;14(13):1295-1306.

    Not in our library10.1016/s1470-2045(13)70491-1

  179. 179.

    Zhang Y, Pan T, Zhong X, Cheng C. Nicotine upregulates microRNA-21 and promotes TGF-β-dependent epithelial-mesenchymal transition of esophageal cancer cells. Tumour Biol. 2014;35(7):7063-7072.

    Not in our library10.1007/s13277-014-1968-z

  180. 180.

    Zhang Y, Yan LX, Wu QN, Du ZM, Chen J, Liao DZ, et al. miR-125b is methylated and functions as a tumor suppressor by regulating the ETS1 proto-oncogene in human invasive breast cancer. Cancer Res. 2011;71(10):3552-3562.

    Not in our library10.1158/0008-5472.can-10-2435

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