Environmental Chemical Exposures Research Articles

Environmental chemicals exposure and abnormal expression of non-coding RNAs

Environmental chemicals exposure is closely related to occurrence and development of diseases. The abnormal expression of non-coding RNAs is a key factor in biological effects of environmental chemicals. Non-coding RNAs play an important role in the normal function of cells and the occurrence and development of diseases. In addition, non-coding RNAs, as a biomarker, could be widely used in the diagnosis, prevention and treatment of diseases. This paper outlines the relationship between environmental chemical exposure and non-coding RNAs and the function and mechanism of non-coding RNAs. It also presents existing issues and future research directions.

Socioeconomic position and exposure to multiple environmental chemical contaminants in six European mother-child cohorts.

Human exposure to environmental chemical contaminants at critical periods of development can lead to lifelong health consequences. Traditionally, socioeconomically disadvantaged groups are thought to experience higher contaminant exposures; however, this relationship may not hold for all contaminants. Using data from six European birth cohorts (1301 mother-child pairs), we determined biomarkers of exposure to 41 contaminants in biological samples from children (6-12 years) and their mothers during pregnancy, including organochlorine compounds (OCs), polybrominated diphenyl ethers (PBDEs), per- and polyfluoroalkyl substances (PFASs), metals, phthalate metabolites, phenols, and organophosphate (OP) pesticide metabolites. We analyzed these biomarkers with several socioeconomic position (SEP) indicators (maternal education, employment status and family affluence scale). Higher SEP was associated with higher concentrations of several chemicals during pregnancy, including certain PFASs, mercury, arsenic, several phenols, and OP pesticides. Similarly, childhood concentrations of OCs, PFASs, mercury, arsenic, and bisphenol A were higher in higher SEP groups. Conversely, cadmium exposure during pregnancy and exposure to lead and phthalate metabolites in childhood were higher in lower SEP. Principal components representing multiple pollutant exposures showed similar association with SEP. This study demonstrates that environmental chemical contaminant exposure during fetal and childhood life is not exclusively associated to lower SEP and that for several contaminants higher SEP groups incur higher exposure levels.

Adenomatous polyposis coli as a predictor of environmental chemical-induced transgenerational effects related to male infertility.

Exposure to toxic environmental chemicals during pregnancy is a ubiquitous threat to health with potentially transgenerational consequences. However, the underlying mechanism of how transgenerational effects occur as part of environmental chemical exposure are not well understood. We investigated the potential molecular changes associated with dibutyl phthalate exposure that induced transgenerational effects, using a rat model. Through the analysis of the Gene Expression Omnibus database, we found some similar studies of environmental exposure induced transgenerational effects. Then, we analyzed one of the studies and our results to identify the adenomatous polyposis coli (APC) gene. This gene participated the most of the pathways and was upregulated in both studies. We used the miRWALK data set to predict the microRNAs which targeted the APC gene. We confirmed the miR-30 family were significantly downregulated in F3 testis tissues and targeted the APC gene. In conclusion, the miR-30 family/APC interaction is a potential mechanism for the transgenerational effects induced by the environmental chemical.

Peak Exposures in Epidemiologic Studies and Cancer Risks: Considerations for Regulatory Risk Assessment.

We review approaches for characterizing “peak” exposures in epidemiologic studies and methods for incorporating peak exposure metrics in dose–response assessments that contribute to risk assessment. The focus was on potential etiologic relations between environmental chemical exposures and cancer risks. We searched the epidemiologic literature on environmental chemicals classified as carcinogens in which cancer risks were described in relation to “peak” exposures. These articles were evaluated to identify some of the challenges associated with defining and describing cancer risks in relation to peak exposures. We found that definitions of peak exposure varied considerably across studies. Of nine chemical agents included in our review of peak exposure, six had epidemiologic data used by the U.S. Environmental Protection Agency (US EPA) in dose–response assessments to derive inhalation unit risk values. These were benzene, formaldehyde, styrene, trichloroethylene, acrylonitrile, and ethylene oxide. All derived unit risks relied on cumulative exposure for dose–response estimation and none, to our knowledge, considered peak exposure metrics. This is not surprising, given the historical linear no‐threshold default model (generally based on cumulative exposure) used in regulatory risk assessments. With newly proposed US EPA rule language, fuller consideration of alternative exposure and dose–response metrics will be supported. “Peak” exposure has not been consistently defined and rarely has been evaluated in epidemiologic studies of cancer risks. We recommend developing uniform definitions of “peak” exposure to facilitate fuller evaluation of dose response for environmental chemicals and cancer risks, especially where mechanistic understanding indicates that the dose response is unlikely linear and that short‐term high‐intensity exposures increase risk.

Establishment and depletion of the ovarian reserve: physiology and impact of environmental chemicals.

The reproductive life span in women starts at puberty and ends at menopause, following the exhaustion of the follicle stockpile termed the ovarian reserve. Increasing data from experimental animal models and epidemiological studies indicate that exposure to a number of ubiquitously distributed reproductively toxic environmental chemicals (RTECs) can contribute to earlier menopause and even premature ovarian failure. However, the causative relationship between environmental chemical exposure and earlier menopause in women remains poorly understood. The present work, is an attempt to review the current evidence regarding the effects of RTECs on the main ovarian activities in mammals, focusing on how such compounds can affect the ovarian reserve at any stages of ovarian development. We found that in rodents, strong evidence exists that in utero, neonatal, prepubescent and even adult exposure to RTECs leads to impaired functioning of the ovary and a shortening of the reproductive lifespan. Regarding human, data from cross-sectional surveys suggest that human exposure to certain environmental chemicals can compromise a woman's reproductive health and in some cases, correlate with earlier menopause. In conclusion, evidences exist that exposure to RTECs can compromise a woman's reproductive health. However, human exposures may date back to the developmental stage, while the adverse effects are usually diagnosed decades later, thus making it difficult to determine the association between RTECs exposure and human reproductive health. Therefore, epidemiological surveys and more experimental investigation on humans, or alternatively primates, are needed to determine the direct and indirect effects caused by RTECs exposure on the ovary function, and to characterize their action mechanisms.

Environmental chemical exposures among Greenlandic children in relation to diet and residence

ABSTRACT The objective of this study was to identify geographic, dietary, and other predictors for childhood exposure to perfluoroalkyl substances (PFASs), polychlorinated biphenyls (PCBs), and methylmercury in Greenlandic children. The study includes cross-sectional data from 367 Greenlandic children aged 7 to 12 years examined during 2012–2015. A parent or guardian participated in a structured interview, and a blood sample from the child was analysed for PFASs, PCBs and total mercury. Predictors for the environmental exposures were identified using linear regression. Area of residence was found to have the strongest explanatory power, accounting for 24% to 68% of the variance in the serum concentrations. Information about diet was available for two-thirds of the children, and among these, consumption of traditional Greenlandic food accounted for 2% to 10% of the variance in the biomarker concentrations. Models including all predictors associated with at least one of the environmental chemicals explained 19% to 54% of the total variance. In conclusion, area is a likely proxy for a traditional marine diet, and together area and diet constitute the most important predictors of exposure to methylmercury, PCBs and PFASs among Greenlandic children.

A Toxicogenomic Approach Reveals a Novel Gene Regulatory Network Active in In Vitro and In Vivo Models of Thyroid Carcinogenesis.

Epidemiological and experimental studies emphasize the link between environmental chemicals exposure and thyroid cancer. However, this association is strongly debated and the mechanisms of action of environmental thyroid carcinogens still need to be identified. The analysis of in vitro transcriptomic data developed to investigate the effects of chlorpyrifos on immortalized thyrocytes highlighted the impaired expression of genes involved in endodermal carcinogenesis. This endodermal carcinogenic gene-network (ECGN, including Zfp36l2, Dmbt1, Ddit4), was validated in cellular and mouse models of thyroid carcinogenesis, characterized by the constitutive activation of the mitogen-activated protein kinase (MAPK) pathway and in immortalized thyrocytes exposed to tetrachlorodibenzo-p-dioxin (TCDD) and chlorpyrifos (CPF). The mRNA levels of Zfp36l2, Dmbt1 and Ddit4 were increased in models characterized by MAPK activation or following TCDD exposure, whereas they were inhibited by CPF exposure. Overall, the ECGN transcripts identify a novel gene-regulatory network associated with thyroid carcinogenesis promoted by genetic mutation or by environmental carcinogens. The latter have opposite effects on the modulation of the ECGN transcripts according to their mechanisms of action in promoting carcinogenesis. Therefore, the analyses of ECGN might be helpful in discriminating compounds that promote cellular survival associated or not to proliferation of thyrocytes.

Community health perceptions and human environmental exposure to chromium contamination in a small New Jersey City.

Following a 1983 chromic acid (hexavalent chromium [CrVI]) spill from a Garfield, NJ electroplating plant, CrVI-contaminated water was found in a local firehouse basement in 1993. An ATSDR public health advisory was issued for the plant site in 2010, and from 2008-2015, fourteen residential properties have required remediation to address CrVI-contaminated dust in the basements. As part of the Community Outreach and Engagement Core of the NYU NIEHS Center, seventytwo Garfield residents aged 18-65 years, participated in a community survey with the goal of identifying concerns related to environmental and community health. Thirty-two percent responded that they 'didn't know' if they were exposed to chemicals or pollutants where they live. This finding suggests a limited awareness of environmental chemical exposures, chromium contamination and/or potential exposure to CrVI. Furthermore, toenail clippings were collected from forty-seven Garfield residents and analyzed for total chromium levels to assess potential long-term exposure. On average, residents living on/inside the contaminated plume area had higher total chromium levels in their toenail clippings than residents living outside the plume area. However, chromium levels for all participants were within the range of historical normal. This study highlights the value of partnerships between environmentally-impacted community's and academic scientists working together to identify potential contaminant exposures and address public health concerns through research and environmental health education.

GSTM1 gene expression and copy number variation in prostate cancer patients—Effect of chemical exposures and physical activity

BackgroundMany etiological factors have been related to prostate cancer (CaP) development, progression, and survival, such as age, population origin, geographic area, occupational exposures, and nutrition and lifestyle factors. However, physical activity affords health benefits to cancer patients, including those with CaP. Glutathione S-Transferases enzymes have been linked to CaP because of their role in the detoxification of a wide variety of potential carcinogens, steroid hormones and xenobiotics. Among the different glutathione S-transferases isoforms, null genotype for GSTM1 has been associated with an increased risk of CaP, although data are controversial. As the relationship between copy number variation and gene expression of GSTM1 in CaP remains unexplored, this study analyzed GSTM1 gene expression and/or dosage effect on CaP risk and aggressiveness. The potential protective role of physical activity was also explored. MethodsThree hundred and seventeen patients (159 non-CaP and 158 CaP) were recruited from the Service of Urology (Hospital Virgen de las Nieves, Granada, Spain) over the period 2012 to 2014 and were followed-up until January 2018 to ensure a correct classification of control and patients. Individuals were classified in each group based on histological analysis of tissue biopsy, along with data on PSA level, Gleason score and T stage in patients with biopsies positive for CaP. Individuals with a negative biopsy were considered as controls. All controls underwent a systematic 20-core ultrasound guided biopsy in order to limit the false negative rate. Genomic DNA was extracted from peripheral blood to determine the exact copy numbers of GSTM1, and RNA was extracted from prostate tissue samples to determine GSTM1 gene expression. Both analyses were performed using the qPCR method. A questionnaire was administered to all patients to assess environmental exposures, lifestyle, and physical activity. The association of GSTM1 copy number variation and expression with the rest of variables was assessed by chi-square test and the Mann-Whitney test. Multiple logistic regression was used to assess which factors were associated with the risk of CaP. ResultsThe presence of 1 or 2 copies of the GSTM1 gene was not less prevalent in CaP compared to non-CaP patients; however, a significant decreased GSTM1 gene expression was observed in CaP tissue relative to non-CaP tissue (P = 0.003). CaP patients with environmental exposure to dust and smoke, and smoking habit had a significantly decreased GSTM1 gene expression (and near-significantly decreased for living in urban areas) as compared to non-CaP patients with the same exposures. In addition, physical activity was significantly associated with a lower risk of CaP (P = 0.006) and with increased GSTM1 gene expression (P = 0.002). ConclusionsA reduced GSTM1 gene expression in prostate tissue was observed in CaP patients with some environmental chemical exposures. Intriguingly, physical activity might play a protective role against CaP development, possibly as a result of increasing GSTM1 gene expression in prostate tissue. However, this observation warrants further confirmation.

An overview of environmental chemical exposures and neurodevelopmental impairments in children

Children are widely viewed as the population subgroup that is most vulnerable to the toxicities that result from exposure to environmental chemicals. Their enhanced vulnerability is due to a variety of behavioral and physiologic factors. For many chemicals, the central nervous system (CNS) is the most sensitive target organ. In general, the impacts depend on a chemical’s mode of action, the dose, and the stage of development at which exposure occurs. This paper surveys the toxicology of environmental chemicals, specifically the impacts on children’s intellectual development. It focuses on metals (or metalloids), including mercury, lead, arsenic, fluoride, as well as on pesticides, air pollution, synthetic organic chemicals, and endocrine disruptors. The final section discusses issues germane to estimating the global burden of disease associated with exposures to neurotoxic environmental chemicals.

Incidental Finding of Bladder Cancer in a Young Patient Undergoing Presacral Neurectomy

Objective: Bladder cancer is the most common urinary tract malignancy, however, rare in patients younger than 60 with a median age at diagnosis of 71 in women. Risk factors include smoking, environmental chemical exposure, chronic cystitis, HPV. Although extremely rare, bladder cancer can be seen in children and young adults. We present a case of a 24 yo G0 with longstanding chronic pelvic pain, endometriosis, and interstitial cystitis with an incidental finding of bladder cancer at the time of surgery.

182 - Time-course metabolomic analysis of manganese toxicity reveals biomarkers of oxidative stress and amino acid metabolism as early cellular targets

Manganese (Mn) is a naturally occurring essential nutrient at low doses that functions as a cofactor in multiple enzymatic reactions, provides structural stability and participates in redox activities. However, high Mn exposure even under federal safety limits for air Mn levels, may cause a dose-dependent progression of Parkinsonism. The molecular mechanisms and critical transitions from normal Mn physiology to low dose toxicity as well as early targets of Mn toxicity nonetheless remains poorly understood. In this temporal study, we used human neuroblastoma SH-SY5Y cells exposed to Mn concentrations varied over a physiologic (5μM MnCl2) and toxicological range (50μM MnCl2) for 0, 0.5, 2, 5 and 10h (n=9 per Mn concentration and time point). Metabolomics analysis was done using liquid chromatography with ultra-high resolution mass spectrometry and cellular Mn accumulation was measured using ICP-MS. Results showed cellular Mn accumulation increased upto 5h in a dose dependent manner, beyond which Mn uptake was stabilized. Pathway enrichment analysis showed that methionine and cysteine metabolism; urea cycle metabolism; glycine, serine, alanine and threonine metabolism; and histidine metabolism were significantly altered within 30min of manganese treatment and persisted upto 10h suggesting these pathways define early targeted mechanisms of Mn toxicity. Discriminatory metabolites involved in methionine and cysteine pathway include methionine, homocysteine, 1,2 dihydroxy-3-keto-5-methylthiopentene and 5’-methylthioadenosine. Discriminatory metabolites involved in glycine, serine, alanine and threonine metabolism include 3-phosphohydroxypyruvate, phosphoserine, serine and creatine. These early responders may reflect rapid transport and redistribution of Mn within the cell. In conclusion, we demonstrate key metabolic biomarkers and pathways that respond dynamically to varying Mn concentration and attempt to provide a chronological fingerprint of Mn dependent toxicity. Time course metabolomics thereby provides a useful tool to predict metabolic status for dynamic systems at the cellular level in response to environmental chemical exposures.

The developmental basis of disease: Update on environmental exposures and animal models.

At the Prenatal Programming and Toxicity (PPTox) Conference I in 2008, I presented an overview of the developmental origins of health and disease field focusing on environmental chemical exposures and disease outcomes. At that time, I noted that the field was getting off the ground with a focus on developmental exposure to a small number of endocrine disrupting chemicals (EDCs) and disease outcomes across the lifespan in animal models. In this update, I note that the DOHaD field has changed significantly over the last decade. There are new windows of susceptibility including preconception, prepuberty, a focus on the mother and not just the offspring, and a significant focus on the new field of epigenetic transgenerational inheritance. New disease focus areas have sprung up including obesity, type 2 diabetes and fatty liver disease, all with a connection to developmental exposures to EDCs. There is also a focus on the study of new EDCs, molecular mechanisms, the development of new biomarkers of exposure and disease outcomes and studies focusing on intervention and prevention studies.

Environmental non-persistent endocrine-disrupting chemicals exposure and reproductive hormones levels in adult men.

Non-persistent endocrine-disrupting chemicals (EDCs) are exogenous, man-made substances present in the environment that may interfere with the natural human hormones and may exert adverse consequences on human organism. Endocrinedisrupting chemicals have been suspected to be associated with altered reproductive function in the case of males and females. Environmental endocrine-disrupting non-persistent chemicals like parabens, phthalates, bisphenol A (BPA), synthetic pyrethroids and organophosphate pesticides are found in various products such as metal food cans, plastic bottles, detergents, personal care products or chemicals used for fighting against insects. The widespread distribution of these chemicals causes that humans are permanently exposed through multiple sources. The aim of this review is to summarize data linking non-persistent endocrine-disrupting chemicals exposure, and human, male reproductive hormones levels. The included studies were selected by searched PubMed, Web of Science and MEDLINE, original papers published from 2006 to 2016 and referring to human data were included to the review. The results of reviewed studies were not consistent, however, majority of the studies indicated that non-persistent EDCs may affect male reproductive hormones levels. Most findings suggest that exposure to environmental EDCs is negatively related to the level of testosterone (except for exposure to BPA which is positively associated). In most of the studies negative association was found between exposure to examined EDCs and free androgen index, too. Considering the suggested health effect of exposure to EDCs, more epidemiological data is needed. Int J Occup Med Environ Health 2018;31(5):551-573.

Free access platforms for integrating environmental chemical exposure and hazard information

How does the world crystallise from quantum weirdness? We might just have heard the answer, says Bob Henderson

Children's Environmental Health in Thailand: Past, Present, and Future.

Background:There is increasing evidence of a link between environmental pollution and preventable diseases in developing countries, including Thailand. Economic development has generated several types of pollution that can affect population health. While these environmental health effects can be observed throughout life, pregnant women and children represent particularly vulnerable and sensitive groups.Methods:The published epidemiological literature investigating environmental chemical exposure in Thai children was reviewed, highlighting those that investigated associations between exposure and subsequent health outcomes.Results:The majority of the Thai epidemiological studies on environmental health in children were cross-sectional in design, with some demonstrating associations between exposure and outcome. The three main types of chemical exposure in Thai children were pesticides, heavy metals, and air pollution, which resulted from agricultural activities in countryside areas, industrial zones (both registered and unregistered establishments), mining, and traffic in inner cities. Major health outcomes included detrimental effects on cognitive function and cancer risk. Pesticide exposure was focused on, but not limited to, agricultural areas. The success of the Thai environmental policy to introduce lead–free petrol can be demonstrated by the decline of mean blood lead levels in children, particularly in urban areas. However, unregistered lead-related factories and smelters act as hidden sources. In addition, there is increasing concern, but little acknowledgement, about the effects of chronic arsenic exposure related to mining. Lastly, air pollution remains a problem in both dense city populations due to traffic and in rural areas due to contamination of indoor air and house dust with heavy metals, endotoxins and other allergens.Conclusions:The increasing number of published articles demonstrates an improved awareness of children’s environmental health in Thailand. Chemical hazards, including the improper use of pesticides, environmental contamination with heavy metals (lead and arsenic), and air pollution in inner cities and indoor air, continue to be growing issues.

Using bisphenol A and its analogs to address the feasibility and usefulness of the CALUX-PPARγ assay to identify chemicals with obesogenic potential

Environmental chemical exposures have been implicated in the obesity epidemic as potential mis-regulators of a variety of metabolic pathways. As agonism of the peroxisome proliferator-activated nuclear hormone receptor γ (PPARγ) is one of the suspected mechanisms involved, a PPARγ screening assay may have relevance for the biodetection of such effects of environmental chemicals. To test this hypothesis, we established the PPARγ2-CALUX® assay in-house and tested it against a number of known and suspected PPARγ modulators. Furthermore, we added a rat liver S9 metabolizing system to the protocol to introduce metabolic competence to the assay. Our results confirmed the responsiveness of the cell line to the known PPARγ agonists and antagonists: rosiglitazone, tributyltin, 15-deoxy-Δ12,14-prostaglandin J2, GW9662 and diclofenac. These data are in agreement with previous studies in various models. Seven bisphenol analogs tested induced little to no agonist activity, but all demonstrated antagonistic properties. These findings were contrary to both our assumptions and literature reports. Addition of the S9-metabolizing system to each of these tests did not alter any of the measured activities. Taken together, it seems probable that there are additional obesogenic effects of these chemicals which would not be detected by this assay.

Profiles and Predictors of Environmental Chemical Mixture Exposure among Pregnant Women: The Health Outcomes and Measures of the Environment Study.

Pregnant women are exposed to numerous environmental chemicals, but there is limited understanding of chemical mixture exposure profiles and predictors. In a prospective cohort of 389 pregnant women from Cincinnati, OH, we used biomarkers to estimate exposure to 41 phenols, phthalates, metals, organophosphate/pyrethroid/organochlorine pesticides, polychlorinated biphenyls, polybrominated diphenyl ethers, perfluoroalkyl substances, and environmental tobacco smoke. Using pairwise correlations, k-means clustering, and principal component analysis (PCA), we identified several profiles of chemical exposure. Chemicals within structurally, commercially, or industrially related chemical classes (e.g., phthalates) were moderate to strongly correlated compared to unrelated chemicals (e.g., pyrethroid pesticides and environmental tobacco smoke). Using k-means clustering and PCA, we identified 3 clusters of women ( N = 106, 158, and 125) and 6 PC scores, respectively, that characterized profiles of cumulative chemical exposure. The first two PC scores significantly varied by cluster, indicating that some of these profiles could be identified using both methods. Cluster membership and PCA scores were associated with race, marital status, consumption of fresh fruits and vegetables, and parity. Future work could use clusters and PCA scores to characterize environmental chemical mixture exposures in other cohorts of pregnant women and predict potential health effects of environmental chemical mixture exposure.

Environmental Endocrine Disruptors and Neurological Disorders

We live in a world where daily exposure to environmental chemicals is inevitable. Many studies point to environmental chemicals a major cause of neurological diseases. Properly intervening in and managing the exposure requires up-to-date information about neurotoxic chemicals that may lead to neurological disorders. The recent literature on the neurotoxic effects of environmental chemicals was reviewed, including both animal and human studies. Parkinson’s disease, Alzheimer’s disease and autism are closely associated with environmental chemicals such as polychlorinated biphenys (PCBs), dioxins, polybrominated biphenyl ethers (PBDE), and perfluoroalkyls. There is strong evidence linking environmental chemical exposure to neurodevelopmental and neurodegenerative diseases. In particular, it is important to pay close attention to a high risk-age group where the window of exposure is critical to causing neurological disease. Key Words: Alzheimer disease, Parkinson disease, Neurotoxic chemicals, Endocrine disruptors

Diazinon exposure activated transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ) and induced adipogenesis in 3T3-L1 preadipocytes

Environmental chemical exposure could be a contributor to the increasing obesity epidemic. Diazinon, an organophosphate insecticide, has been widely used in the agriculture, and exposure of the general population to diazinon has been reported. Diazinon has been known to induce neurotoxic effects mainly through the inhibition of acetylcholinesterase (AChE). However, its association with dysregulation of adipogenesis has been poorly investigated. The current study aimed to examine the mechanism of diazinon's effect on adipogenesis using the 3T3-L1 preadipocytes combined with a single-cell-based high-content analysis. The results showed that diazinon induced lipid droplet accumulation in a dose-dependent manner. The dynamic changes of adipogenic regulatory proteins and genes were examined at the three stages of adipogenesis (induction, differentiation, and maturation) in 3T3-L1 cells treated with various doses of diazinon (0, 1, 10, 100 μM) using real-time quantitative RT-PCR and Western Blot respectively. Diazinon significantly induced protein expression of transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), their downstream proteins, fatty acid synthase (FASN), acetyl CoA carboxylase (ACC), fatty acid-binding protein 4 (FABP4), lipoprotein lipase (LPL), adiponectin and perilipin in dose and time-dependent manners. Similarly, the adipogenic genes were significantly induced in a dose and time-dependent manner compared to the relative controls. The current study demonstrates that diazinon promotes lipid accumulation and activates the adipogenic signaling pathway in the in vitro model.