Many emerging infectious diseases in human populations are associated with zoonotic origins. Attention has often focused on wild animal reservoirs, but most zoonotic pathogens of recent concern to ...human health either originate in, or are transferred to, human populations from domesticated animals raised for human consumption. Thus, the ecological context of emerging infectious disease comprises two overlapping ecosystems: the natural habitats and populations of wild animals, and the anthropogenically controlled habitats and populations of domesticated species. Intensive food animal production systems and their associated value chains dominate in developed countries and are increasingly important in developing countries. These systems are characterized by large numbers of animals being raised in confinement with high throughput and rapid turnover. Although not typically recognized as such, industrial food animal production generates unique ecosystems—environments that may facilitate the evolution of zoonotic pathogens and their transmission to human populations. It is often assumed that confined food animal production reduces risks of emerging zoonotic diseases. This article provides evidence suggesting that these industrial systems may increase animal and public health risks unless there is recognition of the specific biosecurity and biocontainment challenges of the industrial model. Moreover, the economic drivers and constraints faced by the industry and its participants must be fully understood in order to inform preventative policy. In order to more effectively reduce zoonotic disease risk from industrial food animal production, private incentives for the implementation of biosecurity must align with public health interests.
Background: Previous reviews have shown increases in blood pressure and hypertension associated with increases in lead levels in blood. We performed a meta-analysis of the association of bone lead ...levels with systolic blood pressure, diastolic blood pressure, and hypertension using published data. Methods: We searched Medline, Embase, and Toxline for epidemiologic studies on bone lead levels and blood pressure endpoints. We used inverse-variance weighted random-effects models to summarize the association of tibia or patella lead levels with blood pressure endpoints. Results: We summarized data from 3 prospective studies and 5 cross-sectional studies. All studies measured lead levels in tibia bone and 3 studies measured lead levels in patella. For a 10 μg/g increase in tibia lead, the cross-sectional summary increases in blood pressure were 0.26 mm Hg for systolic (95% confidence interval = 0.02 to 0.50) and 0.02 mm Hg for diastolic (-0.15 to 0.19). The summary odds ratio for hypertension was 1.04 (1.01 to 1.07). For a 10 μg/g increase in patella lead, the summary odds ratio for hypertension was 1.04 (0.96 to 1.12). Conclusion: Systolic blood pressure and hypertension risk were associated with lead levels in tibia bone, but the magnitude of the summary estimates was small. These summary estimates, however, were based on published data and we could not evaluate nonlinear dose-response relationships, the relative contribution of bone and blood lead levels, or the influence of differences in study populations. A more detailed characterization of the association of bone lead levels and blood pressure endpoints would require a pooled analysis of individual participant data from existing studies.
While the problem of unsafe tap water in Flint, Michigan fueled outrage and better awareness in regard to the hazards of lead in tap water, the problem has existed in city after city for years in the ...US and in other countries. Our author, a winner of the MacArthur Foundation "genius" grant for her work in identifying preventable causes of human disease related to environmental exposures, points out that problems extend well beyond lead. Many potentially harmful contaminants have yet to be evaluated, much less regulated. Her article examines a number of neurotoxins and related issues as they pertain to brain development.
Mercury is a widespread environmental contaminant with neurotoxic impacts that have been observed over a range of exposures. In addition, there is increasing evidence that inorganic mercury (iHg) and ...organic mercury (including methyl mercury) have a range of immunotoxic effects, including immune suppression and induction of autoimmunity. In this study, we investigated the effect of iHg on a model of autoimmune heart disease in mice induced by infection with coxsackievirus B3 (CVB3). We examined the role of timing of iHg exposure on disease; in some experiments, mice were pretreated with iHg (200 μg/kg, every other day for 15 days) before disease induction with virus inoculation, and in others, they were treated with iHg after the acute (viral) phase of disease but before the development of dilated cardiomyopathy (DCM). iHg alone had no effect on heart pathology. Pretreatment with iHg before CVB3 infection significantly increased the severity of chronic myocarditis and DCM compared with control animals receiving vehicle alone. In contrast, treatment with iHg after acute myocarditis did not affect the severity of chronic disease. The increased chronic myocarditis, fibrosis, and DCM induced by iHg pretreatment were not due to increased viral replication in the heart, which was unaltered by iHg treatment. iHg pretreatment induced a macrophage infiltrate and mixed cytokine response in the heart during acute myocarditis, including significantly increased interleukin (IL)-12, IL-17, interferon-γ, and tumor necrosis factor-α levels. IL-17 levels were also significantly increased in the spleen during chronic disease. Thus, we show for the first time that low-dose Hg exposure increases chronic myocarditis and DCM in a murine model.
Characterizing the risks posed by nanomaterials is extraordinarily complex because these materials can have a wide range of sizes, shapes, chemical compositions and surface modifications, all of ...which may affect toxicity. There is an urgent need for a testing strategy that can rapidly and efficiently provide a screening approach for evaluating the potential hazard of nanomaterials and inform the prioritization of additional toxicological testing where necessary. Predictive toxicity models could form an integral component of such an approach by predicting which nanomaterials, as a result of their physico-chemical characteristics, have potentially hazardous properties. Strategies for directing research towards predictive models and the ancillary benefits of such research are presented here.
Methylmercury (MeHg) is a ubiquitous environmental contaminant with known neurodevelopmental effects. In humans, prenatal exposures primarily occur through maternal consumption of contaminated fish. ...In this study, we evaluated the association between prenatal exposure to MeHg and titers of total immunoglobulins (Ig) and specific autoantibodies in both mothers and fetuses by analyzing maternal and cord blood serum samples. We examined multiple immunoglobulin isotypes to determine if these biomarkers could inform as to fetal or maternal responses since IgG but not IgM can cross the placenta. Finally, we evaluated serum cytokine levels to further characterize the immune response to mercury exposure.
The study was conducted using a subset of serum samples (
N=61 pairs) collected from individuals enrolled in a population surveillance of MeHg exposures in the Brazilian Amazon during 2000/2001. Serum titers of antinuclear and antinucleolar autoantibodies were measured by indirect immunofluorescence. Serum immunoglobulins were measured by enzyme-linked immunosorbent assay (ELISA) and BioPlex multiplex assay. Serum cytokines were measured by BioPlex multiplex assay.
In this population, the geometric mean mercury level was within the 95th percentile for US populations of women of childbearing age but the upper level of the range was significantly higher. Fetal blood mercury levels were higher (1.35 times) than those in their mothers, but highly correlated (correlation coefficient
r=0.71; 95% CI: 0.54, 0.89). Total IgG (
r=0.40; 95% CI: 0.19, 0.62) and antinuclear autoantibody (odds ratio OR=1.05; 95% CI: 1.02, 1.08) levels in paired maternal and fetal samples were also associated; in contrast, other immunoglobulin (IgM, IgE, and IgA) levels were not associated between pairs. Total IgG levels were significantly correlated with both maternal (
r=0.60; 95% CI: 0.25, 0.96) and cord blood mercury levels (
r=0.61; 95% CI: 0.25, 0.97), but individual isotypes were not. Serum cytokines, interleukin-1β (
r=0.37; 95% CI: 0.01, 0.73), interleukin-6 (
r=0.34; 95% CI: 0.03, 0.65), and tumor necrosis factor-α (
r=0.24; 95% CI: 0.015, 0.47), were positively correlated between maternal and fetal samples. Antinuclear and antinucleolar autoantibody titer and serum cytokine levels, in either maternal or cord blood, were not significantly associated with either maternal or cord blood mercury levels.
These data provide further evidence that there are likely IgG biomarkers of mercury-induced immunotoxicity in this population since IgG levels were elevated with increased, and associated with, mercury exposure. However, unlike previous data from adult males and non-pregnant females, we found no evidence that antinuclear and antinucleolar autoantibody titer is a reliable biomarker of mercury immunotoxicity in this population.
► In a cross-sectional study, we examine prenatal immune responses to mercury. ► IgG, autoantibodies, and cytokines were measured in maternal and fetal blood. ► Maternal mercury level was predicted by the number of fish meals per day. ► Fetal IgG was increased with mercury exposure, but not autoantibody or cytokine.
The localization and intensification of the poultry industry over the past 50 years have incidentally created a largely ignored environmental management crisis. As a result of these changes in ...poultry production, concentrated animal feeding operations (CAFOs) produce far more waste than can be managed by land disposal within the regions where it is produced. As a result, alternative waste management practices are currently being implemented, including incineration and pelletization of waste. However, organic arsenicals used in poultry feed are converted to inorganic arsenicals in poultry waste, limiting the feasibility of waste management alternatives. The presence of inorganic arsenic in incinerator ash and pelletized waste sold as fertilizer creates opportunities for population exposures that did not previously exist. The removal of arsenic from animal feed is a critical step toward safe poultry waste management.
A database for studies used for U.S. Environmental Protection Agency (EPA) pesticide and chemical reviews would be an excellent resource for increasing transparency and improving systematic ...assessments of pesticides and chemicals. There is increased demand for disclosure of raw data from studies used by the U.S. EPA in these reviews.
Because the Information Quality Act (IQA) of 2001 provides an avenue for request of raw data, we reviewed all IQA requests to the U.S. EPA in 2002-2012 and the U.S. EPA's responses. We identified other mechanisms to access such data: public access databases, the Freedom of Information Act (FOIA), and reanalysis by a third party.
Only two IQA requests to the U.S. EPA were for raw data. Both of these were fulfilled under FOIA, not the IQA. Barriers to the U.S. EPA's proactive collection of all such data include costs to the U.S. EPA and researchers, significant time burdens for researchers, and major regulatory delays. The U.S. EPA regulatory authority in this area is weak, especially for research conducted in the past, not funded by the U.S. government, and/or conducted abroad. The U.S. EPA is also constrained by industry confidential business information (CBI) claims for regulatory testing data under U.S. chemical and pesticide laws. The National Institutes of Health Clinical Trials database systematically collects statistical data about clinical trials but not raw data; this database may be a model for data from studies of chemicals and pesticides.
A database that registers studies and obtains systematic sets of parameters and results would be more feasible than a system that attempts to make all raw data available proactively. Such a proposal would not obviate rights under the IQA to obtain raw data at a later point.
Environmental risk factors (defined as those agents and stresses that are generally the responsibility of environmental agencies) are often tangible indicators of economic and social disparity in the ...United States. Many site-specific analyses have reported that communities of color and poverty are exposed more often and more intensively to such environmental hazards as lead, air pollution, agrochemicals, incinerator emissions, and releases from hazardous waste sites. Thus, exposures to these toxicants may explain part of the socioeconomic disparity that is observed in terms of risks of adverse pregnancy outcomes. The purpose of this study was to describe the associations between certain environmental exposures and reproductive outcomes through a discussion of both epidemiologic and animal model studies. In addition, we list potential sources of exposure data and describe physiologic changes in pregnancy that may increase the likelihood of both external exposures and increased internal dose. Several models for further study of environmental risk factors are suggested to increase our understanding of gene-environment interactions toward the goal of indentifying preventable risk factors to improve reproductive outcomes of particular concern to disadvantaged populations.
While methicillin-resistant Staphylococcus aureus (MRSA) originally was associated with healthcare, distinct strains later emerged in patients with no prior hospital contact. The epidemiology of MRSA ...continues to evolve.
To characterize the current epidemiology of MRSA-colonized patients entering a hospital serving both rural and urban communities, we interviewed patients with MRSA-positive admission nasal swabs between August 2009 and March 2010. We applied hospitalization risk factor, antimicrobial resistance phenotype, and multi-locus sequence genotype (MLST) classification schemes to 94 case-patients.
By MLST analysis, we identified 15 strains with two dominant clonal complexes (CCs)-CC5 (51 isolates), historically associated with hospitals, and CC8 (27 isolates), historically of community origin. Among patients with CC5 isolates, 43% reported no history of hospitalization within the past six months; for CC8, 67% reported the same. Classification by hospitalization risk factor did not correlate strongly with genotypic classification. Sensitivity of isolates to ciprofloxacin, clindamycin, or amikacin was associated with the CC8 genotype; however, among CC8 strains, 59% were resistant to ciprofloxacin, 15% to clindamycin, and 15% to amikacin.
Hospitalization history was not a strong surrogate for the CC5 genotype. Conversely, patients with a history of hospitalization were identified with the CC8 genotype. Although ciprofloxacin, clindamycin, and amikacin susceptibility distinguished CC8 strains, the high prevalence of ciprofloxacin resistance limited its predictive value. As CC8 strains become established in healthcare settings and CC5 strains disseminate into the community, community-associated MRSA definitions based on case-patient hospitalization history may prove less valuable in tracking community MRSA strains.
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