The primary goal of solid waste management to protect the health of the population, particularly low-income groups, has been hindered by lack of local data to pinpoint priorities and identify ...appropriate interventions across African cities. To fill this gap in order to inform policy and action, this paper examines different levels of exposure to solid waste dumpsites and associated health outcomes in Nairobi, Kenya and Dakar, Senegal. Using representative survey data of households, the study found higher primary exposure of households to the major dumpsite in Nairobi than in Dakar (70% versus 33%, respectively), following the physical proximity of Nairobi municipal dumpsite to large settlements. While there are higher levels of perception of risks to health associated with exposure to dumpsites in Nairobi than Dakar, the linkages between levels of exposure to dumpsites and incidences of morbidities (diarrhea/cholera and respiratory infections) was consistent in the two cities. The protective roles of gender and age of household head in Dakar and the net implications of socio-economic differences, highlight context-specific inputs needed in policy and program interventions. The low incidences of morbidity in Dakar than Nairobi provide empirical evidence supporting the negative health implications of siting dumpsites close to human settlements.
The widespread use of pesticides to control agricultural pests is a hot topic on the public scene of environmental health. Selective pest control for minimum environmental impact is a major goal of ...the environmental toxicology field, notably to avoid unintended poisoning in different organisms. Anticoagulant rodenticides cause abnormal blood coagulation process; they have been widely used to control rodents, allowing inadvertent primary and secondary exposure in domestic animals and non-target predatory wildlife species through direct ingestion of rodenticide-containing bait or by consumption of poisoned prey. To report toxic effect, the most common approach is the measurement of liver or plasma residues of anticoagulant rodenticides in dead or intoxicated animals showing clinical symptoms. However, one major challenge is that literature currently lacks a hepatic or plasma concentration threshold value for the differentiation of exposure from toxicity. Regarding the variation in pharmacology properties of anticoagulant rodenticides inter- and intra-species, the dose-response relationship must be defined for each species to prejudge the relative risk of poisoning. Beyond that, biomarkers are a key solution widely used for ecological risk assessment of contaminants. Since anticoagulant rodenticides (AR) have toxic effects at the biochemical level, biomarkers can serve as indicators of toxic exposure. In this sense, toxicological knowledge of anticoagulant rodenticides within organisms is an important tool for defining sensitive, specific, and suitable biomarkers. In this review, we provide an overview of the toxicodynamic and toxicokinetic parameters of anticoagulant rodenticides in different animal species. We examine different types of biomarkers used to characterize and differentiate the exposure and toxic effects of anticoagulant rodenticide, showing the strengths and weaknesses of the assays. Finally, we describe possible new biomarkers and highlight their capabilities.
Background: Two novel systemic inflammation indices, SII and SIRI, are associated with increased risk of cardiovascular diseases (CVD). However, SII and SIRI are prone to change over time and the ...association between changeable status and long-term outcome risk remains to be uncovered. This study aims to examine the association between the dynamic status of SII and SIRI and risk of CVD. Methods: This prospective study included a total of 45,809 subjects without MI, stroke and cancer prior to or in 2010 (baseline of this study). The dynamic status of SII and SIRI during 2006, 2008, and 2010 was assessed by dynamic trajectories (primary exposure), annual increase, and average value. The outcome was CVD incidence during 8.6 years' follow-up. Multiple Cox regression models were used to calculate the adjusted hazard ratios (HRs) and confidence intervals (95% CIs). Results: Four dynamic trajectories of SII and SIRI were identified as follows: low stable pattern, moderate stable pattern, increase pattern, and decrease pattern. For SII, compared with "low stable pattern", after controlling confounders and level of SII in 2006, adjusted HRs were 1.24 (95% CI = 1.02-1.51) for "increase pattern" and 1.11 (95% CI = 1.00-1.23) for "moderate-stable pattern" while the association was not significant for "decrease pattern". Additionally, the highest group of annual SII increase and average SII had respective HR of 1.20 (95% CI = 1.05-1.37) and 1.32 (95% CI = 1.13-1.55). The results were consistent for SIRI. "Increase pattern" and "moderate stable pattern" increased the risk of CVD by 38% (HR = 1.38, 95% CI = 1.17-1.63) and 12% (HR = 1.12, 95% CI = 1.01-1.25), while no significant association was found for "decrease pattern". The highest group of annual SIRI increase and average SIRI had respective HR of 1.25 (95% CI = 1.09-1.44) and 1.39 (95% CI = 1.19-1.63). Conclusion: Dynamic status of SII and SIRI was significantly associated with risk of CVD, which highlighted that we should focus on the dynamic change of SII and SIRI. Keywords: systemic inflammation, dynamic status, prospective study, cardiovascular diseases
Vitellogenin (vtg) is a precursor of the yolk proteins lipovitelline and phosvitin and is synthesized as a consequence of estrogen-dependent gene expression in female and male hepatocytes of ...egg-laying vertebrates. Freshly isolated carp hepatocytes of a genetically uniform strain of adult male carp (Cyprinus carpio) were used to investigate the effects of primary exposure to estrogenic compounds on the vitellogenic response to xenoestrogens. Isolated carp hepatocytes were first exposed (primary exposure) to 50 or 100 μM of either methoxychlor (MXCL) or bisphenol A (BPA), different concentrations of estrone (E1; 1 or 10 nM) or 17β-estradiol (E2; 0.1 or 1 nM) for 2 days. Hepatocytes were exposed to xenoestrogens (secondary exposure) at both 2 and 5 days after isolation. Hepatocytes were cultured for a total period of 8 days. A competitive indirect ELISA was used to determine the level of vtg after 8 days. The concentration of chemicals used for the primary exposure induced vtg to a level that was less than 10% of the response elicited by E2 (1000 nM). A cytotoxic response, measured by MTT, was not observed after primary exposure to any of the xenoestrogens. After primary exposure to MXCL, vtg production in response to E2 was increased by 4-fold, and vitellogenesis in response to E1 treatment was doubled compared with vitellogenesis without pretreatment. No significant differences were observed between primary exposure to 50 and 100 μM MXCL. Primary exposure to 50 and 100 μM BPA increased the maximum vtg production in response to secondary E2 exposure by about 5- and 7-fold, respectively. Primary exposure to BPA (50 and 100μM) followed by secondary exposure to E1 showed a 4- and 5-fold increase of the vtg synthesis in comparison to E1 exposure alone. Primary exposure to the endogenous estrogens had no significant influence on the vtg synthesis in response to secondary exposure to E1 or E2. Compared to hepatocytes exposed only to MXCL or BPA, primary exposure to E2 increased the vtg synthesis in hepatocytes induced by MXCL or BPA by almost a factor of 2. Primary exposure to E1 increased vitellogenesis after secondary exposure to MXCL only marginally. The present results indicate that weakly estrogenic environmental chemicals such as MXCL and BPA can increase the sensitivity of carp hepatocytes towards endogenous estrogens with respect to VTG synthesis.
SUMMARY
The polymorphic domain of the gene encoding Plasmodium falciparum merozoite surface protein 2 (MSP2) was PCR amplified from blood of malaria patients, genotyped, and 19 distinct fragments ...were cloned and expressed in E. coli. The reactivity of naturally occurring antibodies against this panel of recombinant MSP2 antigens was tested using 67 homologous or heterologous sera from a serum bank of travel clinic patients. Sera from semi‐immune individuals strongly recognized almost all recombinant antigens. Sera from primary infected patients either did not react at all (9 sera), or reacted weakly against varying numbers of antigens (39 sera). The antigens that showed reactions were mostly of the allelic family corresponding to the infecting clone, but in very few cases also of the alternative allelic family. Single clone infections and repeated samples from the same individual were analysed in greater detail. Thus, we were able to quantify cross‐reactivity induced by a single P. falciparum infection. Within the two allelic families of MSP2, cross‐reactivity was observed between some but not all alleles of the same family, whereas antibodies cross‐reactive between variants belonging to different allelic families were detected in only a few cases.
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