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The Lancet. Neurology Mar 2014Neurodevelopmental disabilities, including autism, attention-deficit hyperactivity disorder, dyslexia, and other cognitive impairments, affect millions of children... (Review)
Review
Neurodevelopmental disabilities, including autism, attention-deficit hyperactivity disorder, dyslexia, and other cognitive impairments, affect millions of children worldwide, and some diagnoses seem to be increasing in frequency. Industrial chemicals that injure the developing brain are among the known causes for this rise in prevalence. In 2006, we did a systematic review and identified five industrial chemicals as developmental neurotoxicants: lead, methylmercury, polychlorinated biphenyls, arsenic, and toluene. Since 2006, epidemiological studies have documented six additional developmental neurotoxicants-manganese, fluoride, chlorpyrifos, dichlorodiphenyltrichloroethane, tetrachloroethylene, and the polybrominated diphenyl ethers. We postulate that even more neurotoxicants remain undiscovered. To control the pandemic of developmental neurotoxicity, we propose a global prevention strategy. Untested chemicals should not be presumed to be safe to brain development, and chemicals in existing use and all new chemicals must therefore be tested for developmental neurotoxicity. To coordinate these efforts and to accelerate translation of science into prevention, we propose the urgent formation of a new international clearinghouse.
Topics: Animals; Brain; Developmental Disabilities; Environmental Exposure; Humans; Methylmercury Compounds; Neurotoxicity Syndromes; Polychlorinated Biphenyls
PubMed: 24556010
DOI: 10.1016/S1474-4422(13)70278-3 -
Translational Psychiatry Feb 2014Although the involvement of genetic abnormalities in autism spectrum disorders (ASD) is well-accepted, recent studies point to an equal contribution by environmental... (Review)
Review
Although the involvement of genetic abnormalities in autism spectrum disorders (ASD) is well-accepted, recent studies point to an equal contribution by environmental factors, particularly environmental toxicants. However, these toxicant-related studies in ASD have not been systematically reviewed to date. Therefore, we compiled publications investigating potential associations between environmental toxicants and ASD and arranged these publications into the following three categories: (a) studies examining estimated toxicant exposures in the environment during the preconceptional, gestational and early childhood periods; (b) studies investigating biomarkers of toxicants; and (c) studies examining potential genetic susceptibilities to toxicants. A literature search of nine electronic scientific databases through November 2013 was performed. In the first category examining ASD risk and estimated toxicant exposures in the environment, the majority of studies (34/37; 92%) reported an association. Most of these studies were retrospective case-control, ecological or prospective cohort studies, although a few had weaker study designs (for example, case reports or series). Toxicants implicated in ASD included pesticides, phthalates, polychlorinated biphenyls (PCBs), solvents, toxic waste sites, air pollutants and heavy metals, with the strongest evidence found for air pollutants and pesticides. Gestational exposure to methylmercury (through fish exposure, one study) and childhood exposure to pollutants in water supplies (two studies) were not found to be associated with ASD risk. In the second category of studies investigating biomarkers of toxicants and ASD, a large number was dedicated to examining heavy metals. Such studies demonstrated mixed findings, with only 19 of 40 (47%) case-control studies reporting higher concentrations of heavy metals in blood, urine, hair, brain or teeth of children with ASD compared with controls. Other biomarker studies reported that solvent, phthalate and pesticide levels were associated with ASD, whereas PCB studies were mixed. Seven studies reported a relationship between autism severity and heavy metal biomarkers, suggesting evidence of a dose-effect relationship. Overall, the evidence linking biomarkers of toxicants with ASD (the second category) was weaker compared with the evidence associating estimated exposures to toxicants in the environment and ASD risk (the first category) because many of the biomarker studies contained small sample sizes and the relationships between biomarkers and ASD were inconsistent across studies. Regarding the third category of studies investigating potential genetic susceptibilities to toxicants, 10 unique studies examined polymorphisms in genes associated with increased susceptibilities to toxicants, with 8 studies reporting that such polymorphisms were more common in ASD individuals (or their mothers, 1 study) compared with controls (one study examined multiple polymorphisms). Genes implicated in these studies included paraoxonase (PON1, three of five studies), glutathione S-transferase (GSTM1 and GSTP1, three of four studies), δ-aminolevulinic acid dehydratase (one study), SLC11A3 (one study) and the metal regulatory transcription factor 1 (one of two studies). Notably, many of the reviewed studies had significant limitations, including lack of replication, limited sample sizes, retrospective design, recall and publication biases, inadequate matching of cases and controls, and the use of nonstandard tools to diagnose ASD. The findings of this review suggest that the etiology of ASD may involve, at least in a subset of children, complex interactions between genetic factors and certain environmental toxicants that may act synergistically or in parallel during critical periods of neurodevelopment, in a manner that increases the likelihood of developing ASD. Because of the limitations of many of the reviewed studies, additional high-quality epidemiological studies concerning environmental toxicants and ASD are warranted to confirm and clarify many of these findings.
Topics: Child Development Disorders, Pervasive; Gene-Environment Interaction; Hazardous Substances; Humans
PubMed: 24518398
DOI: 10.1038/tp.2014.4 -
Journal of Environmental Science and... 2013Polychlorinated biphenyls (PCBs) are toxic and persistent chemicals produced between 1930s and 1980s primarily for insulating fluids in heavy-duty electrical equipment... (Meta-Analysis)
Meta-Analysis Review
Polychlorinated biphenyls (PCBs) are toxic and persistent chemicals produced between 1930s and 1980s primarily for insulating fluids in heavy-duty electrical equipment in power plants, industries, and large buildings. They persist in the environment and accumulate in plants and animals, and have been classified as probable carcinogens to humans. We performed a systematic review and meta-analysis of scientific literature on the relationship between PCB exposure and human cancer. Two cohorts of people highly exposed to PCBs through ingestion of contaminated rice oil and some cohorts of occupationally exposed workers failed to show a definite increase in total cancer mortality and provided inconsistent results regarding single cancers. Several cohort and case-control studies investigated the association between PCBs and specific cancers, showing an association between PCB serum levels and non-Hodgkin lymphomas (NHL), with a summary odds ratio of 1.5 (95% confidence interval: 1.1-1.7), but no consistent results for the other cancer sites and types. In conclusion, this review provides some evidence for the role of PCBs in the development of NHL, although the inconsistent results of studies performed on highly polluted people and occupationally exposed workers do not allow a firm conclusion to be drawn.
Topics: Carcinogens; Case-Control Studies; Cohort Studies; Environmental Exposure; Food Contamination; Humans; Incidence; Neoplasms; Occupational Exposure; Polychlorinated Biphenyls
PubMed: 23672403
DOI: 10.1080/10590501.2013.782174 -
Environment International Feb 2013Disruption of developing immune and respiratory systems by early-life exposure to persistent organic pollutants (POPs) could result into reduced capacity to fight... (Review)
Review
BACKGROUND
Disruption of developing immune and respiratory systems by early-life exposure to persistent organic pollutants (POPs) could result into reduced capacity to fight infections and increased risk to develop allergic manifestations later in life.
OBJECTIVES
To systematically review the epidemiologic literature on the adverse effects of early-life exposure to POPs on respiratory health, allergy and the immune system in infancy, childhood and adolescence.
METHODS
Based on published guidelines for systematic reviews, two independent researchers searched for published articles in MEDLINE and SCOPUS using defined keywords on POPs and respiratory health, immune function and allergy. Study eligibility criteria were defined to select the articles.
RESULTS
This review of 41 studies finds limited evidence for prenatal exposure to DDE, PCBs and dioxins and risk of respiratory infections. Evidence was limited also for postnatal exposure to PCBs, specifically ndl-PCBs, and reduced immune response after vaccination in childhood. The review indicates lack of association between postnatal exposure to PCBs/ndl-PCBs and risk of asthma-related symptoms. For the other exposure-outcome associations reviewed evidence was inadequate.
DISCUSSION AND CONCLUSION
Current epidemiological evidence suggests that early-life exposure to POPs can adversely influence immune and respiratory systems development. Heterogeneity between studies in exposure and outcome assessment and the small number of studies for any given exposure-outcome relationship currently make comparisons difficult and meta-analyses impossible. Also, mechanisms remain largely unexplored. Recommendations for significantly improving our understanding thus include harmonization of exposure and outcome assessment between studies, conduct of larger studies, long-term assessment of respiratory infections and asthma symptoms in order to identify critical periods of susceptibility, integration of the potential immunotoxic mechanisms of POPs, and use of new statistical tools to detangle the role of multiple exposures on multiple outcomes.
Topics: Asthma; Dichlorodiphenyl Dichloroethylene; Dioxins; Hazardous Substances; Humans; Hypersensitivity; Immune System; Polychlorinated Biphenyls; Respiratory System; Respiratory Tract Infections
PubMed: 23291098
DOI: 10.1016/j.envint.2012.11.005 -
Chemosphere Apr 2013There is reasonably strong evidence linking reduced secondary sex ratio (proportion of males) and environmental exposures. Polychlorinated biphenyls (PCBs) are... (Review)
Review
There is reasonably strong evidence linking reduced secondary sex ratio (proportion of males) and environmental exposures. Polychlorinated biphenyls (PCBs) are persistent contaminants of the environment and several studies have reported an association of PCBs with birth outcomes. A decrease in the male/female sex ratio at birth has been reported in some, but not all studies. The aim of this systematic review was to summarize and pool the research findings about the influence of PCBs on sex ratio. Several article databases and reference lists of identified articles were searched. Studies reporting the proportion of boys and girls born to individuals who were exposed to high PCB concentrations were included. The primary outcome measure was the proportion of males in groups exposed to high or low levels of PCBs. Studies with both direct and indirect surrogate PCB measurements were included. The search and selection resulted in 15 eligible studies on the association between the sex ratio and parental PCB exposures. Analyses of the high exposure groups showed that the sex ratio was not significantly altered from the historical reference range in 13 of the 15 articles. The majority of the exposure studies reported also internal comparisons between high and low PCB exposure levels. The pooled 95% confidence interval estimate for the difference in high and low maternal exposure with direct PCB measure was - 0.048 with 95% CI of (-0.121, 0.026). There was no strong or moderate indication that parental exposure to PCBs alters the sex ratio of the children.
Topics: Environmental Pollutants; Environmental Pollution; Female; Humans; Male; Maternal Exposure; Polychlorinated Biphenyls; Sex Ratio
PubMed: 23260246
DOI: 10.1016/j.chemosphere.2012.11.019 -
Environment International Oct 2011Numerous studies analyzed concentrations of persistent organic pollutants (POPs) in human samples, and in many types of foods; however, food consumption is less commonly... (Review)
Review
BACKGROUND
Numerous studies analyzed concentrations of persistent organic pollutants (POPs) in human samples, and in many types of foods; however, food consumption is less commonly included in studies on the determinants of POP concentrations in humans, and these approaches are rarely integrated with surveys of food intake to estimate the amount and safety of human POP intake from food.
OBJECTIVE
To analyze the main characteristics and findings of all studies conducted in Spain that quantitatively assessed the influence of diet on human concentrations of POPs.
METHODS
Studies published until December 2010 (with no other time restrictions) were identified through Medline/PubMed, ISI-Thomson, ScienceDirect, and SciELO databases.
RESULTS
We identified 25 papers, from 19 different studies. Twelve papers were published in 2009-2010. All studies but one were based on subgroups not representative of the general population, and over half were limited to women. Serum was the most used biological matrix, while p,p'-DDE, HCB and PCBs were the most frequently analyzed compounds. Food intakes were measured with heterogeneous food frequency questionnaires. The most consistent association was between fish consumption and PCBs and HCB, followed by dairy products and PCBs. A few studies observed a relationship between meat and some POPs, whilst intake of vegetables, fruits and cereals was rarely related to POP levels. Only 3 studies did not find any relationship between dietary habits and POP concentrations.
CONCLUSIONS
In spite of methodological heterogeneity, the studies were able to quantify to what extent consumption of foods from animal origin (fish, milk, dairy products and meat) is related to higher body concentrations of POPs. As in a few other countries, in Spain food consumption is increasingly analyzed as a major determinant of human POP intake.
Topics: Animals; Dairy Products; Dichlorodiphenyl Dichloroethylene; Diet; Diet Surveys; Environmental Exposure; Environmental Pollutants; Food Analysis; Hexachlorobenzene; Humans; Meat; Organic Chemicals; Polychlorinated Biphenyls; Seafood; Spain
PubMed: 21683445
DOI: 10.1016/j.envint.2011.05.008 -
Emerging Health Threats Journal Apr 2011More than 100 studies have examined whether environmental or occupational exposures of parents affect the sex ratio of their offspring at birth. For this review, we...
More than 100 studies have examined whether environmental or occupational exposures of parents affect the sex ratio of their offspring at birth. For this review, we searched Medline and Web of Science using the terms 'sex ratio at birth' and 'sex ratio and exposure' for all dates, and reviewed bibliographies of relevant studies to find additional articles. This review focuses on exposures that have been the subject of at least four studies including polychlorinated biphenyls (PCBs), dioxins, pesticides, lead and other metals, radiation, boron, and g-forces. For paternal exposures, only dioxins and PCBs were consistently associated with sex ratios higher or lower than the expected 1.06. Dioxins were associated with a decreased proportion of male births, whereas PCBs were associated with an increased proportion of male births. There was limited evidence for a decrease in the proportion of male births after paternal exposure to DBCP, lead, methylmercury, non-ionizing radiation, ionizing radiation treatment for childhood cancer, boron, or g-forces. Few studies have found higher or lower sex ratios associated with maternal exposures. Studies in humans and animals have found a reduction in the number of male births associated with lower male fertility, but the mechanism by which environmental hazards might change the sex ratio has not yet been established.
PubMed: 24149027
DOI: 10.3402/ehtj.v4i0.7109 -
The Mount Sinai Journal of Medicine,... 2010Practitioners see a large number of children affected by environmental exposures each year. A national network of pediatric environmental health specialty units has been... (Review)
Review
BACKGROUND
Practitioners see a large number of children affected by environmental exposures each year. A national network of pediatric environmental health specialty units has been established to strengthen prevention capacity, yet the effectiveness of that translational resource has not been assessed.
METHODS
We supplemented a qualitative systematic review of previous assessments of healthcare provider capacity with a self-administered survey sent to the membership of the Michigan chapter of the American Academy of Pediatrics. We mailed surveys twice between October 2007 and January 2008 and obtained a 39.4% response rate.
RESULTS
Our systematic review identified 8 relevant studies, all of which relied on self-report questionnaires and surveys. Recognizing this methodological weakness, we found that national and state samples consistently identified significant gaps in self-efficacy and knowledge about environmental hazards across a broad range of child care providers. In the Michigan survey, respondents voiced high self-efficacy in dealing with lead and second-hand smoke, but confidence in managing pesticide, mercury, mold, polychlorinated biphenyl, and air pollution exposures was much lower (P < 0.0001). Pediatricians routinely referred affected patients to lead/toxicology clinics and allergist/immunologists but not to the regional pediatric environmental health specialty unit.
CONCLUSIONS
Gaps persist in practitioner knowledge about environmental health nationwide and across disciplines. Despite methodological weaknesses, educational opportunities and other efforts should be studied to determine best practices for enhancing the evaluation of environmental health concerns in children.
Topics: Asthma; Child; Developmental Disabilities; Diffusion of Innovation; Environmental Exposure; Environmental Health; Female; Health Care Surveys; Humans; Lead Poisoning; Male; Michigan; Middle Aged; Practice Patterns, Physicians'; Referral and Consultation; Self Efficacy; United States
PubMed: 20101722
DOI: 10.1002/msj.20158 -
Chemosphere Mar 2009Reported evidence regarding relationships between polychlorinated biphenyls (PCBs) and thyroid homeostasis in adults has been considered contradictory. The objective of... (Review)
Review
Reported evidence regarding relationships between polychlorinated biphenyls (PCBs) and thyroid homeostasis in adults has been considered contradictory. The objective of this systematic review is to determine a possible association between PCB exposure and the circulating thyroid hormones and thyrotropin (TSH) levels in adults, by analyzing the quality of published studies. A systematic review of epidemiological papers was conducted using PubMed. An evaluation of the quality of 22 studies was performed, and the papers were classified into two tiers: Tier I for studies with higher quality scores (eight) and Tier II for studies with lower quality scores (14). It appears that PCBs can interfere with thyroid hormone homeostasis; however epidemiological evidence is not entirely clear. For triiodothyronine (T3) and thyroxine (T4), Tier I studies showed either an inverse (four cases for T3; five cases for T4) or no significant association (two cases for T3; five cases for T4) with PCBs. In the case of free thyroxine and TSH, the Tier I papers observed no clear association with PCB levels. Rigorous study design, assessment of potential confounding factors, and fuller reporting of methods and results in future studies will facilitate understanding of whether PCB exposure is associated with changes in thyroid function.
Topics: Adult; Antithyroid Agents; Confounding Factors, Epidemiologic; Epidemiologic Studies; Female; Homeostasis; Humans; Male; Polychlorinated Biphenyls; Pregnancy; Thyroid Hormones; Thyrotropin; Thyroxine; Triiodothyronine
PubMed: 19108870
DOI: 10.1016/j.chemosphere.2008.11.031 -
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