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Environmental Health : a Global Access... Jul 2017Air pollution is involved in many pathologies. These pollutants act through several mechanisms that can affect numerous physiological functions, including reproduction:... (Review)
Review
BACKGROUND
Air pollution is involved in many pathologies. These pollutants act through several mechanisms that can affect numerous physiological functions, including reproduction: as endocrine disruptors or reactive oxygen species inducers, and through the formation of DNA adducts and/or epigenetic modifications. We conducted a systematic review of the published literature on the impact of air pollution on reproductive function. Eligible studies were selected from an electronic literature search from the PUBMED database from January 2000 to February 2016 and associated references in published studies. Search terms included (1) ovary or follicle or oocyte or testis or testicular or sperm or spermatozoa or fertility or infertility and (2) air quality or O or NO or PM2.5 or diesel or SO or traffic or PM10 or air pollution or air pollutants. The literature search was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We have included the human and animal studies corresponding to the search terms and published in English. We have excluded articles whose results did not concern fertility or gamete function and those focused on cancer or allergy. We have also excluded genetic, auto-immune or iatrogenic causes of reduced reproduction function from our analysis. Finally, we have excluded animal data that does not concern mammals and studies based on results from in vitro culture. Data have been grouped according to the studied pollutants in order to synthetize their impact on fertility and the molecular pathways involved.
CONCLUSION
Both animal and human epidemiological studies support the idea that air pollutants cause defects during gametogenesis leading to a drop in reproductive capacities in exposed populations. Air quality has an impact on overall health as well as on the reproductive function, so increased awareness of environmental protection issues is needed among the general public and the authorities.
Topics: Air Pollutants; Air Pollution; Animals; Female; Gametogenesis; Humans; Infertility; Male; Mammals
PubMed: 28754128
DOI: 10.1186/s12940-017-0291-8 -
Food & Function Oct 2016Epidemiological studies suggest that olive oil intake is associated to a reduced risk of cancer. Recently, the chemopreventive activity of olive oil has been attributed... (Review)
Review
Epidemiological studies suggest that olive oil intake is associated to a reduced risk of cancer. Recently, the chemopreventive activity of olive oil has been attributed to its unique phenolic compounds represented by phenolic alcohols, hydroxytyrosol (3,4-dihydroxyphenylethanol: 3,4-DHPEA) and tyrosol (p-hydroxyphenylethanol: p-HPEA), and their secoiridoid derivatives 3,4-DHPEA-EA (oleuropein aglycon), p-HPEA-EA (ligstroside aglycon), 3,4-DHPEA-EDA, p-HPEA-EDA (oleocanthal), and oleuropein. Several studies have demonstrated that these compounds are able to inhibit proliferation and induce apoptosis in different tumor cell lines. These in vitro effects have been recently summarized in several reviews. The aim of this systematic review was to evaluate the in vivo anti-cancer activities of secoiridoid phenols as evidenced by either animal models of carcinogenesis or human intervention trials. From the literature research through "PubMed" and "Web of Science", 16 animal studies and 5 human intervention trials were identified and included in the review. Most of the animal studies have confirmed the ability of these compounds to inhibit the carcinogenesis process at both initiation and promotion/progression phases. All human intervention trials have investigated the effects of olive oil phenols on DNA damage. Among the five selected studies, three have shown a significant preventive effect on oxidative DNA damage in terms of reduction of 8-oxo-7,8-dihydro-2'-deoxyguanosine in urine, in mitochondria DNA of mononuclear cells and in lymphocyte DNA. The other two studies failed to see an effect on the urinary excretion of either etheno-DNA adducts or oxidation products of guanine. Further investigations are necessary to clarify the real chemopreventive potential of olive oil secoiridoid phenols on humans performing intervention studies on populations at high cancer risk.
Topics: Animals; Antineoplastic Agents, Phytogenic; Humans; Iridoids; Molecular Structure; Olive Oil; Phenols
PubMed: 27713961
DOI: 10.1039/c6fo00958a -
Toxicology Letters Oct 2014A large body of evidence from epidemiological studies among workers employed in the rubber manufacturing industry has indicated a significant excess cancer risk in a... (Review)
Review
A large body of evidence from epidemiological studies among workers employed in the rubber manufacturing industry has indicated a significant excess cancer risk in a variety of sites. The International Agency for Research on Cancer has recently classified the "Occupational exposures in the rubber-manufacturing industry" as carcinogenic to humans (Group 1). A genotoxic mechanism for the increased cancer risk was suggested on the basis of the evidence from the scientific literature. Exposure assessment studies have shown that workers in the rubber manufacturing industry may be exposed to different airborne carcinogenic and/or genotoxic chemicals, such as certain aromatic amines, polycyclic aromatic hydrocarbons, N-nitrosamines, although the available information does not allow to establish a causal association of cancer or genotoxic risk with particular substances/classes of chemicals or specific jobs. The aim of this paper is to critically evaluate, by conducting a systematic review, the available biomonitoring studies using genotoxicity biomarkers in rubber manufacturing industry. This systematic review suggests that a genotoxic hazard may still be present in certain rubber manufacturing industries. A quantitative risk assessment needs further studies addressing the different, processes and chemicals in the rubber manufacturing industries.
Topics: Chromosome Aberrations; DNA Adducts; DNA Damage; Environmental Monitoring; Humans; Manufacturing Industry; Mutation; Occupational Exposure; Risk Assessment; Rubber
PubMed: 24275385
DOI: 10.1016/j.toxlet.2013.11.013 -
Occupational and Environmental Medicine Sep 2012The association between ambient air pollution exposure and lung cancer risk has been investigated in prospective studies and the results are generally consistent,... (Review)
Review
The association between ambient air pollution exposure and lung cancer risk has been investigated in prospective studies and the results are generally consistent, indicating that long-term exposure to air pollution may cause lung cancer. Despite the prospective nature and consistent findings of these studies, causality assessment can benefit from biomarker research. In the present systematic review, we assess the contribution of intermediate biomarkers in epidemiological studies, to ascertain whether their measurement reinforces causal reasoning. We have reviewed 524 papers which described the relationships between ambient air pollution and biological markers of dose and early response. The evidence for each marker was evaluated using assessment criteria which rate a group of studies from A (strong) to C (weak) on amount of evidence, replication of findings, and protection from bias. Biomarkers that scored A or B for all three criteria are included here. The markers that fulfilled the inclusion criteria are: 1-hydroxypyrene, DNA adducts, chromosomal aberrations, micronuclei, oxidative damage to nucleobases, and methylation changes. These biomarkers cover the whole spectrum of disease onset and progression from external exposure to tumour formation and some have also been suggested as risk predictors of future cancer, reinforcing causal reasoning. However, methodological issues such as confounding, publication bias and use of surrogate tissues instead of target tissues in studies on these markers are of concern. The identified biological markers have potential to shed light on the pathways of carcinogenesis, thus defining the association more clearly for public health interventions.
Topics: Air Pollution; Biomarkers; DNA Adducts; Environmental Exposure; Humans; Lung Neoplasms; Methylation; Micronuclei, Chromosome-Defective; Oxidative Stress; Pyrenes
PubMed: 22773658
DOI: 10.1136/oemed-2011-100566 -
Acta Obstetricia Et Gynecologica... Jan 2011The terrorist explosions of the World Trade Center in New York City and the other events on the Pentagon and in Pennsylvania on 11 September 2001 were stressful events...
BACKGROUND
The terrorist explosions of the World Trade Center in New York City and the other events on the Pentagon and in Pennsylvania on 11 September 2001 were stressful events that affected people around the world. Pregnant women and their offspring are especially vulnerable during and after such a terrorist attack. The objective was to systematically review the risks of adverse pregnancy outcomes after the terrorist attacks on Sept 11, 2001.
METHODS
The Meta-analysis of Observational Studies in Epidemiology (MOOSE) criteria were used for reporting of this review. Statistical analyses were performed using RevMan 5.0.
RESULTS
Ten reports of low-to-moderate risk of methodological bias were included. There was increased risks of infants with birthweight of 1,500 g-1,999 g (adjusted odds ratio [AOR] 1.67 [95%CI 1.11-2.52]) and small-for-gestational age births (AOR 1.90; 95%CI 1.05-3.46) in New York. There was increased risks of low birthweight (relative risk 2.25; 95%CI 1.29-3.90) and preterm births (relative risk 1.50; 95%CI 1.06-2.14) among ethnically Arabic women living in California There was a reduction in birthweight by 276 g and in head circumference by 1 cm when DNA adducts, a marker for environmental toxin exposure, were doubled in maternal blood. In Holland, a 48-g reduction in birthweight was reported.
CONCLUSIONS
The World Trade Center disaster influenced pregnancy outcomes in New York, among ethnically Arab women living in California and among Dutch women. The adverse outcomes are likely due to environmental pollution and stress in New York, ethnic harassment in California and communal bereavement and stress in Holland.
Topics: Female; Humans; Pregnancy; Pregnancy Complications; September 11 Terrorist Attacks
PubMed: 21275910
DOI: 10.1111/j.1600-0412.2010.01020.x -
Environment International Feb 2011Several mechanisms are suspected to underlie adverse birth outcomes among mothers exposed to air pollutants, including inflammation, direct toxic effects on fetuses and... (Review)
Review
BACKGROUND
Several mechanisms are suspected to underlie adverse birth outcomes among mothers exposed to air pollutants, including inflammation, direct toxic effects on fetuses and the placenta, displacement of the oxygen-hemoglobin dissociation curve, and formation of DNA adducts.
OBJECTIVE
To systematically review the association between air pollutants and birth outcomes of low birth weight (LBW), preterm (PTB) and small for gestational age (SGA) births.
METHODS
Electronic databases and bibliographies of identified articles were searched for English language studies reporting on birth outcomes. Included studies were assessed for risks of bias in the selection, exposure assessment, confounder adjustment, analyses, outcomes assessment, and attrition. Unadjusted and adjusted estimates from included studies were extracted. Methodological differences between the studies were evaluated.
RESULTS
A total of 41 studies, mostly with a moderate risk of biases due to indirect assessment methods employed, met the eligibility criteria. Exposure to sulphur dioxide was associated with PTB, exposure to fine particulate matter (PM) of ≤2.5 μM was associated with LBW, PTB and SGA births, and exposure to coarse PM of ≤10 μM was associated with SGA births. The evidence for nitrous oxide, nitrogen dioxide, ozone and carbon monoxide was inconclusive.
CONCLUSIONS
Reported associations, and lack thereof, between individual air pollutants and birth outcomes have differed across published studies. This heterogeneity and/or absence of association may be due to difficulty in quantifying exposure, method of ascertainment, time of measurement and collinearity between pollutants. Important future research directions include developing improved methods to detect the duration and intensity of exposure, including entire populations, as well as performing well-designed nested studies that ascertain complete outcomes, avoiding residual confounding, and adjusting for residential mobility.
Topics: Air Pollutants; Air Pollution; Birth Weight; Female; Gestational Age; Humans; Infant, Low Birth Weight; Infant, Newborn; Inhalation Exposure; Male; Maternal Exposure; Particulate Matter; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Premature Birth; Sulfur Dioxide
PubMed: 21112090
DOI: 10.1016/j.envint.2010.10.009 -
Evidence Report/technology Assessment Nov 2010The purpose of this report is to systematically examine the possible causal mechanism(s) that may explain the association between alcohol (ethanol) consumption and the... (Review)
Review
OBJECTIVES
The purpose of this report is to systematically examine the possible causal mechanism(s) that may explain the association between alcohol (ethanol) consumption and the risk of developing breast and colorectal cancers.
DATA SOURCES
We searched 11 external databases, including PubMed® and Embase, for studies on possible mechanisms. These searches used Medical Subject Headings and free text words to identify relevant evidence.
REVIEW METHODS
Two reviewers independently screened search results, selected studies to be included, and reviewed each trial for inclusion. We manually examined the bibliographies of included studies, scanned the content of new issues of selected journals, and reviewed relevant gray literature for potential additional articles.
RESULTS
Breast Cancer. Five human and 15 animal studies identified in our searches point to a connection between alcohol intake and changes in important metabolic pathways that when altered may increase the risk of developing breast cancer. Alterations in blood hormone levels, especially elevated estrogen-related hormones, have been reported in humans. Several cell line studies suggest that the estrogen receptor pathways may be altered by ethanol. Increased estrogen levels may increase the risk of breast cancer through increases in cell proliferation and alterations in estrogen receptors. Human studies have also suggested a connection with prolactin and with biomarkers of oxidative stress. Of 15 animal studies, six reported increased mammary tumorigenesis (four administered a co-carcinogen and two did not). Other animal studies reported conversion of ethanol to acetaldehyde in mammary tissue as having a significant effect on the progression of tumor development. Fifteen cell line studies suggested the following mechanisms: Increased hormonal receptor levels. Increased cell proliferation. A direct stimulatory effect. DNA adduct formation. Increase cyclic adenosine monophosphate (camp). Change in potassium channels. Modulation of gene expression. Colorectal Cancer. One human tissue study, 19 animal studies (of which 12 administered a co-carcinogen and seven did not), and 10 cell line studies indicate that ethanol and acetaldehyde may alter metabolic pathways and cell structures that increase the risk of developing colon cancer. Exposure of human colonic biopsies to acetaldehyde suggests that acetaldehyde disrupts epithelial tight junctions. Among 19 animal studies the mechanisms considered included: Mucosal damage after ethanol consumption. Increased degradation of folate. Stimulation of rectal carcinogenesis. Increased cell proliferation. Increased effect of carcinogens. Ten cell line studies suggested: Folate uptake modulation. Tumor necrosis factor modulation. Inflammation and cell death. DNA adduct formation. Cell differentiation. Modulation of gene expression. One study used a combination of animal and cell line and suggested intestinal cell proliferation and disruption of cellular signals as possible mechanisms.
CONCLUSIONS
Based on our systematic review of the literature, many potential mechanisms by which alcohol may influence the development of breast or colorectal cancers have been explored but the exact connection or connections remain unclear. The evidence points in several directions but the importance of any one mechanism is not apparent at this time.
Topics: Alcohol Drinking; Animals; Breast Neoplasms; Cell Proliferation; Colorectal Neoplasms; Estrogens; Ethanol; Female; Humans; Male; Mammary Neoplasms, Animal; Oxidative Stress; Prolactin; Receptors, Estrogen; Risk
PubMed: 23126574
DOI: No ID Found -
Journal of Occupational and... Sep 2009Exposure monitoring programs have been used in the aluminum smelter industry for decades to decrease the risk of cancer from exposure to polycyclic aromatic hydrocarbons... (Review)
Review
Exposure monitoring programs have been used in the aluminum smelter industry for decades to decrease the risk of cancer from exposure to polycyclic aromatic hydrocarbons (PAHs). Biological monitoring of PAHs incorporates all routes of exposure. Measuring postshift urinary 1-hydroxypyrene (1OHP), a metabolite of pyrene, determines worker's daily PAH exposures, while measuring DNA adducts reflect chronic exposures to PAHs. We reviewed the scientific literature to identify changes over time in (1) 1OHP levels, (2) DNA adduct levels, and (3) other contributing factors associated with 1OHP and DNA adduct levels in the aluminum smelter industry. No trends were observed in 1OHP and DNA adduct levels. This could be due to variable selection of study populations and poorly identified job tasks that prevent comparison of jobs across plants and times, unassessed worker exposure variability, and the impact of cumulative exposures. Thus, it cannot be demonstrated that the use of biological monitoring to estimate PAH exposures has brought about an exposure reduction in the industry. Future studies should be aimed at follow-up in workplaces where dermal and inhalation exposure interventions have been employed. Inconsistent findings were also observed in the analysis of CYP1A1, GSTM1, and GSTP1 polymorphisms and their effect on biomarker levels.
Topics: Aluminum; Biomarkers; Carcinogens, Environmental; DNA Adducts; Female; Humans; Male; Metallurgy; Occupational Exposure; Polycyclic Aromatic Hydrocarbons; Pyrenes
PubMed: 19629825
DOI: 10.1080/15459620903094810 -
Cancer Dec 2008The incidence of cancer during pregnancy is increasing given the trend for women to postpone childbearing. Knowledge of the potential toxicity and teratogenicity of... (Review)
Review
The incidence of cancer during pregnancy is increasing given the trend for women to postpone childbearing. Knowledge of the potential toxicity and teratogenicity of chemotherapy agents is crucial for patient counseling. Platinum derivatives are active against various malignancies that occur more frequently during pregnancy: melanoma, cervical and ovarian cancers, and lung cancer. The authors of this article performed a systematic review of reports documenting the use of platinum derivatives during pregnancy in the English literature from 1977 through January 2008. Forty-three pregnancies were described: 36 patients received cisplatin, 6 patients received carboplatin, and 1 patient received both drugs. Two fetal malformations occurred after in utero exposure to cisplatin, but the causative link between cisplatin administration and these malformations remains speculative. However, either detectable cisplatin levels or platinum-DNA adducts were observed in neonates who were exposed to platinum derivatives during the third trimester, providing evidence for a late-onset transplacental transfer of these drugs. The administration of platinum derivatives, although feasible during the second and third trimesters of pregnancy, raises concern regarding the transplacental transfer of these drugs in late pregnancy and has unknown short- and long-term effects.
Topics: Abnormalities, Drug-Induced; Antineoplastic Agents; Carboplatin; Cisplatin; Female; Humans; Maternal-Fetal Exchange; Pregnancy; Pregnancy Complications, Neoplastic; Pregnancy Trimester, Third
PubMed: 18985677
DOI: 10.1002/cncr.23935 -
European Journal of Cardio-thoracic... May 2008Platinum-based regimens are the cornerstones of therapy in adjuvant and neoadjuvant management of early stage non-small cell lung cancer (NSCLC). However, the survival... (Review)
Review
Platinum-based regimens are the cornerstones of therapy in adjuvant and neoadjuvant management of early stage non-small cell lung cancer (NSCLC). However, the survival benefit associated with platinum-based chemotherapy is marginal and therefore adequate patient selection is essential. Excision repair cross complementation 1 (ERCC1) is a key-enzyme in the repair of platinum-DNA adducts that has been demonstrated to influence the response to platinum-based therapy. We performed a systematic review of the literature from 1996 to September 2007 on studies that assessed the role of ERCC1 in resected NSCLC. Overall, nine studies were identified. ERCC1 expression has been assessed by mRNA expression (n=5) and/or by protein expression (immunohistochemistry) (n=5). One study assessed ERCC1 status by both methods. In these studies, patients with early stage NSCLC treated by surgery alone survived longer if ERCC1 levels are high (favourable prognostic value of high ERCC1 level). Conversely, patients treated by surgery and who receive chemotherapy, either as adjuvant therapy or for disease relapse, have a better overall survival when ERCC1 levels are low (favourable predictive value of low ERCC1 level). ERCC1 expression might assist in selecting patients who will respond to adjuvant (neoadjuvant) platinum-based chemotherapy. However, further investigation is necessary in order to prospectively confirm these results and to ascertain the most appropriate method of assessment. Thoracic surgeons should participate in this field of research.
Topics: Antineoplastic Agents; Biomarkers; Carcinoma, Non-Small-Cell Lung; Chemotherapy, Adjuvant; DNA Repair; DNA-Binding Proteins; Endonucleases; Humans; Lung Neoplasms; Platinum; Predictive Value of Tests; Survival Rate
PubMed: 18342529
DOI: 10.1016/j.ejcts.2008.01.067