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Neurotoxicology Sep 2022Investigation of the toxicity triggered by chemicals on the human brain has traditionally relied on approaches using rodent in vivo models and in vitro cell models... (Review)
Review
Investigation of the toxicity triggered by chemicals on the human brain has traditionally relied on approaches using rodent in vivo models and in vitro cell models including primary neuronal cultures and cell lines from rodents. The issues of species differences between humans and rodents, the animal ethical concerns and the time and cost required for neurotoxicity studies on in vivo animal models, do limit the use of animal-based models in neurotoxicology. In this context, human cell models appear relevant in elucidating cellular and molecular impacts of neurotoxicants and facilitating prioritization of in vivo testing. The SH-SY5Y human neuroblastoma cell line (ATCC® CRL-2266™) is one of the most used cell lines in neurosciences, either undifferentiated or differentiated into neuron-like cells. This review presents the characteristics of the SH-SY5Y cell line and proposes the results of a systematic review of literature on the use of this in vitro cell model for neurotoxicity research by focusing on organic environmental pollutants including pesticides, 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD), flame retardants, PFASs, parabens, bisphenols, phthalates, and PAHs. Organic environmental pollutants are widely present in the environment and increasingly known to cause clinical neurotoxic effects during fetal & child development and adulthood. Their effects on cultured SH-SY5Y cells include autophagy, cell death (apoptosis, pyroptosis, necroptosis, or necrosis), increased oxidative stress, mitochondrial dysfunction, disruption of neurotransmitter homeostasis, and alteration of neuritic length. Finally, the inherent advantages and limitations of the SH-SY5Y cell model are discussed in the context of chemical testing.
Topics: Adult; Animals; Cell Line, Tumor; Cell Survival; Child; Environmental Pollutants; Flame Retardants; Fluorocarbons; Humans; Neuroblastoma; Neurotoxicity Syndromes; Parabens; Pesticides; Polychlorinated Dibenzodioxins
PubMed: 35914637
DOI: 10.1016/j.neuro.2022.07.008 -
International Journal of Fertility &... 2015Dioxin-related compounds are associated with teratogenic and mutagenic risks in laboratory animals, and result in adverse pregnancy outcomes. However, there were... (Review)
Review
Dioxin-related compounds are associated with teratogenic and mutagenic risks in laboratory animals, and result in adverse pregnancy outcomes. However, there were inconsistent results in epidemiology studies. In view of this difference, we conducted a systematic review and meta-analysis to examine this association and to assess the heterogeneity among studies. Comprehensive literature searches were performed to search for relevant articles published in English up to 15 May 2012. In total, we identified 15 studies which included 9 cohort and 6 case control studies. The Cochrane Q test and index of heterogeneity (I(2)) were used to evaluate heterogeneity. In either cohort studies (I(2)=0.89, p<0.0001) or case control studies (I(2)=0.69, p=0.02), significant heterogeneity of risk estimates were observed. Subgroup analyses found no significant increased risk of adverse pregnancy outcome with air dioxin-related compounds exposure (RR=0.99, 95% CI:0.85-1.16), no significant increased risk of spontaneous abortion (SAB) with exposure to food dioxin-related compounds (RR=1.05, 95% CI:0.80-1.37), higher significant risks of low birth weight (LBW) with exposure to food dioxin-related compounds (RR=1.55, 95% CI:1.24-1.94), and higher significant risks of birth defects with maternal solid contaminants dioxin exposure (OR=1.24, 95% CI:1.19-1.29). In conclusion, more evidences are needed to confirm the association between environmental dioxin-related compounds exposure and pregnancy outcome.
PubMed: 25780516
DOI: 10.22074/ijfs.2015.4174 -
Systematic Reviews Aug 2021Sarcomas are a rare and heterogeneous group of tumors originating from mesenchymal or connective tissue. They represent less than 1% of all adult cancers. The etiology... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Sarcomas are a rare and heterogeneous group of tumors originating from mesenchymal or connective tissue. They represent less than 1% of all adult cancers. The etiology and epidemiology of sarcomas remain understudied and poorly understood. The main objective of our study was to systematically assess the association between various occupational exposures and risk of sarcomas.
METHODS
We performed a systematic literature search using the PubMed, Scopus, EMBASE and Cochrane databases to identify relevant cohort and case-control studies. A meta-analysis method was applied on the incidence and mortality outcomes where the estimate with 95% confidence interval (CI) was obtained.
RESULTS
We included a total of 50 publications in our systematic review and 35 in meta-analysis. For exposures to phenoxy herbicides and chlorophenols, the pooled odds ratio (OR) for sarcoma was 1.85 (95% CI: 1.22, 2.82), based on 16 studies with 2254 participants, while the pooled standardized mortality ratio was 40.93 (95% CI 2.19, 765.90), based on 4 cohort studies with 59,289 participants. For exposure to vinyl chloride monomers the pooled risk ratios for angiosarcoma of the liver and other STS were 19.23 (95% CI 2.03, 182.46) and 2.23 (95 CI 1.55, 3.22) respectively based on 3 cohort studies with 12,816 participants. Exposure to dioxins was associated with an increased STS mortality; the pooled standardized mortality ratio was 2.56 (95% CI 1.60, 4.10) based on 4 cohort studies with 30,797 participants. Finally, woodworking occupation was associated with an increased risk of STS with the pooled OR of 2.16 (95% CI 1.39, 3.36).
CONCLUSIONS
Our findings suggest a positive association between higher exposure to dioxins and increased mortality from STS, between cumulative exposure to vinyl chloride monomers and increased mortality from angiosarcoma of the liver and STS, and between woodworking occupation and STS incidence. These findings were all statistically significant.
Topics: Adult; Cohort Studies; Humans; Incidence; Occupational Diseases; Occupational Exposure; Sarcoma
PubMed: 34389054
DOI: 10.1186/s13643-021-01769-4 -
Environmental Health Perspectives Nov 2008In this systematic review we evaluated the evidence on the association between dioxin exposure and cardiovascular disease (CVD) mortality in humans. (Review)
Review
OBJECTIVE
In this systematic review we evaluated the evidence on the association between dioxin exposure and cardiovascular disease (CVD) mortality in humans.
DATA SOURCES AND EXTRACTION
We conducted a PubMed search in December 2007 and considered all English-language epidemiologic studies and their citations regarding dioxin exposure and CVD mortality. To focus on dioxins, we excluded cohorts that were either primarily exposed to polychlorinated biphenyls or from the leather and perfume industries, which include other cardiotoxic coexposures.
DATA SYNTHESIS
We included results from 12 cohorts in the review. Ten cohorts were occupationally exposed. We divided analyses according to two well-recognized criteria of epidemiologic study quality: the accuracy of the exposure assessment, and whether the exposed population was compared with an internal or an external (e.g., general population) reference group. Analyses using internal comparisons with accurate exposure assessments are the highest quality because they minimize both exposure misclassification and confounding due to workers being healthier than the general population ("healthy worker effect"). The studies in the highest-quality group found consistent and significant dose-related increases in ischemic heart disease (IHD) mortality and more modest associations with all-CVD mortality. Their primary limitation was a lack of adjustment for potential confounding by the major risk factors for CVD.
CONCLUSIONS
The results of this systematic review suggest that dioxin exposure is associated with mortality from both IHD and all CVD, although more strongly with the former. However, it is not possible to determine the potential bias, if any, from confounding by other risk factors for CVD.
Topics: Cardiovascular Diseases; Cohort Studies; Dioxins; Humans
PubMed: 19057694
DOI: 10.1289/ehp.11579 -
Frontiers in Endocrinology 2023Exposure to endocrine-disrupting chemicals (EDCs) during critical neurodevelopmental windows has been associated with the risk of autistic traits. This systematic review...
AIMS
Exposure to endocrine-disrupting chemicals (EDCs) during critical neurodevelopmental windows has been associated with the risk of autistic traits. This systematic review of epidemiological studies examined the association between maternal exposure to EDCs during pregnancy and the risk of autism spectrum disorder (ASD) in the offspring.
METHODS
We searched PubMed, Web of Science, Scopus, and Google Scholar from inception to November 17, 2022, for studies investigating the association between prenatal exposure to EDCs and outcomes related to ASD. Two independent reviewers screened studies for eligibility, extracted data, and assessed the risk of bias. The review was registered in PROSPERO (CRD42023389386).
RESULTS
We included 27 observational studies assessing prenatal exposure to phthalates (8 studies), polychlorinated biphenyls (8 studies), organophosphate pesticides (8 studies), phenols (7 studies), perfluoroalkyl substances (6 studies), organochlorine pesticides (5 studies), brominated flame retardants (3 studies), dioxins (1 study), and parabens (1 study). The number of examined children ranged from 77 to 1,556, the age at the assessment of autistic traits ranged from 3 to 14 years, and most studies assessed autistic traits using the Social Responsiveness Scale. All but one study was considered to have a low risk of bias. Overall, there was no association between maternal exposure to specific ECDs during pregnancy and the occurrence of autistic traits in offspring.
CONCLUSIONS
Findings from the epidemiological studies evaluated here do not support an association between prenatal exposure to ECDs and the likelihood of autistic traits in later in life. These findings should not be interpreted as definitive evidence of the absence of neurodevelopment effects of EDCs affecting ASD risk, given the limitations of current studies such as representative exposure assessment, small sample sizes, inadequacy to assess sexually dimorphic effects, or the effects of EDC mixtures. Future studies should carefully address these limitations.
Topics: Child; Pregnancy; Female; Humans; Adolescent; Child, Preschool; Endocrine Disruptors; Autism Spectrum Disorder; Prenatal Exposure Delayed Effects; Autistic Disorder; Pesticides; Epidemiologic Studies
PubMed: 37361542
DOI: 10.3389/fendo.2023.1184546 -
Occupational Medicine (Oxford, England) Dec 2017The waste and recycling sector is a growing part of industry. Whether health surveillance is indicated and how it should be undertaken is unclear. (Review)
Review
BACKGROUND
The waste and recycling sector is a growing part of industry. Whether health surveillance is indicated and how it should be undertaken is unclear.
AIMS
To undertake a review of the literature to identify hazards to health, biological effects and occupational illnesses for workers in the sector.
METHODS
A systematic review of the published literature and two UK databases.
RESULTS
Rates of fatal, non-fatal injuries and self-reported work-related illness were found to be higher in the waste and recycling sector than in UK industry as a whole. There was an increased prevalence of respiratory, gastro-intestinal and skin complaints in workers exposed to compost relative to controls. They may also be at increased risk of extrinsic allergic alveolitis, allergic bronchopulmonary aspergillosis, occupational asthma and abnormalities of lung function. Workers involved with the recycling of batteries and cables may be at risk of lead poisoning and exposure to other heavy metals. There were case reports of mercury poisoning from the recycling of fluorescent lights. Cases of occupational asthma have been reported in association with wood and paper recycling. The recycling of e-waste may cause exposure to heavy metals and organic pollutants, such as polybrominated diphenyl ethers, dioxins and polyaromatic hydrocarbons, which have been associated with damage to DNA and adverse neonatal outcomes.
CONCLUSIONS
Ill-health and adverse biological effects have been described in waste and recycling workers, but their true prevalence has probably not been captured. Targeted health surveillance may be required to assess exposure and to identify occupational illness.
Topics: Humans; Manufacturing Industry; Occupational Diseases; Prevalence; Recycling; Waste Disposal Facilities; Workforce
PubMed: 29165683
DOI: 10.1093/occmed/kqx153 -
Epidemiology and Health 2022Various toxic substances can be generated from incinerators, exposing nearby residents, and epidemiological studies have shown wide variations in risk estimates for... (Meta-Analysis)
Meta-Analysis
OBJECTIVES
Various toxic substances can be generated from incinerators, exposing nearby residents, and epidemiological studies have shown wide variations in risk estimates for cancer risk in populations living close to incinerators.
METHODS
Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, a literature search and systematic review were conducted to identify studies conducted on general populations exposed to environmental incinerator emissions and cancer outcomes. Meta-analysis was performed according to the cancer types for which 2 or more studies were reported. Subgroup analysis was done for sex, the exposure estimation method, the study period, and the type of outcome.
RESULTS
Eleven studies were found for the qualitative review and meta-analysis. Seven studies had a case-control design, and 4 had a cohort design. The pooled effect size was not significant for breast, colorectal, liver, lung, lymphohematopoietic, stomach, bladder, central nervous system, and laryngeal cancers, non-Hodgkin lymphoma, sarcoma, leukemia, and all cancers. In the subgroup analysis, the pooled effect size of laryngeal cancer in females was 1.82 (95% confidence interval, 1.10 to 3.01), although only 2 studies were identified.
CONCLUSIONS
The meta-analysis did not provide evidence of an increased risk for any cancer among populations living near waste incinerators, except for laryngeal cancer in females. However, since relatively few studies were reviewed and some cancer types showed significant increases in individual studies, this evidence needs to be updated regularly.
Topics: Female; Humans; Laryngeal Neoplasms; Environmental Exposure; Incineration; Cohort Studies; Case-Control Studies
PubMed: 36097807
DOI: 10.4178/epih.e2022070 -
Environmental Health Perspectives Jul 2021Growing epidemiological evidence suggests that organochlorine chemicals (OCCs), including 2,3,7,8-tetrachlorodibenzo--dioxin (TCDD), may play a role in the pathogenesis...
BACKGROUND
Growing epidemiological evidence suggests that organochlorine chemicals (OCCs), including 2,3,7,8-tetrachlorodibenzo--dioxin (TCDD), may play a role in the pathogenesis of endometriosis.
OBJECTIVES
We aimed to systematically review the experimental evidence ( and ) on the associations between exposure to OCCs and endometriosis-related end points.
METHODS
A systematic review protocol was developed following the National Toxicology Program /Office of Health Assessment and Translation (NTP/OHAT) framework and managed within a web-based interface. studies designed to evaluate the impact of OCCs on the onset or progression of endometriosis and proliferation of induced endometriotic lesions were eligible. Eligible studies included single-cell and co-culture models to evaluate the proliferation, migration, and/or invasion of endometrial cells. We applied the search strings to PubMed, Web of Science, and Scopus®. A final search was performed on 24 June 2020. Assessment of risk of bias and the level of evidence and integration of preevaluated epidemiological evidence was conducted using NTP/OHAT framework Results: Out of 812 total studies, 39 met the predetermined eligibility criteria (15 , 23 , and 1 both). Most studies () tested TCDD and other dioxin-like chemicals. evidence supported TCDD's promotion of endometriosis onset and lesion growth. evidence supported TCDD's promotion of cell migration and invasion, but there was insufficient evidence for cell proliferation. evidence further supported the roles of the aryl hydrocarbon receptor and matrix metalloproteinases in mediating steroidogenic disruption and inflammatory responses. Estrogen interactions were found across studies and end points.
CONCLUSION
Based on the integration of a high level of animal evidence with a moderate level of epidemiological evidence, we concluded that TCDD was a known hazard for endometriosis in humans and the conclusion is supported by mechanistic evidence. Nonetheless, there is need for further research to fill in our gaps in understanding of the relationship between OCCs and their mixtures and endometriosis, beyond the prototypical TCDD. https://doi.org/10.1289/EHP8421.
Topics: Animals; Cell Culture Techniques; Cell Proliferation; Dioxins; Endometriosis; Environmental Exposure; Female; Humans; Hydrocarbons, Chlorinated; Polychlorinated Dibenzodioxins
PubMed: 34310196
DOI: 10.1289/EHP8421 -
Environmental Health : a Global Access... Jan 2011Continuous exposure to many chemicals, including through air, water, food, or other media and products results in health impacts which have been well assessed, however... (Review)
Review
BACKGROUND
Continuous exposure to many chemicals, including through air, water, food, or other media and products results in health impacts which have been well assessed, however little is known about the total disease burden related to chemicals. This is important to know for overall policy actions and priorities. In this article the known burden related to selected chemicals or their mixtures, main data gaps, and the link to public health policy are reviewed.
METHODS
A systematic review of the literature for global burden of disease estimates from chemicals was conducted. Global disease due to chemicals was estimated using standard methodology of the Global Burden of Disease.
RESULTS
In total, 4.9 million deaths (8.3% of total) and 86 million Disability-Adjusted Life Years (DALYs) (5.7% of total) were attributable to environmental exposure and management of selected chemicals in 2004. The largest contributors include indoor smoke from solid fuel use, outdoor air pollution and second-hand smoke, with 2.0, 1.2 and 0.6 million deaths annually. These are followed by occupational particulates, chemicals involved in acute poisonings, and pesticides involved in self-poisonings, with 375,000, 240,000 and 186,000 annual deaths, respectively.
CONCLUSIONS
The known burden due to chemicals is considerable. This information supports decision-making in programmes having a role to play in reducing human exposure to toxic chemicals. These figures present only a number of chemicals for which data are available, therefore, they are more likely an underestimate of the actual burden. Chemicals with known health effects, such as dioxins, cadmium, mercury or chronic exposure to pesticides could not be included in this article due to incomplete data and information. Effective public health interventions are known to manage chemicals and limit their public health impacts and should be implemented at national and international levels.
Topics: Disease; Environmental Pollutants; Environmental Pollution; Epidemiology; Humans; Mortality; Occupational Exposure; Public Health; Public Policy; Risk Assessment
PubMed: 21255392
DOI: 10.1186/1476-069X-10-9