Navigating the aflatoxin and cyanide challenge in traditionally-processed garri: a mechanistic review of cyanide-aflatoxin trade-off, balancing contamination reduction and food safety risks

Food safety risk during the pandemic

Public perceptions and worry about food safety hazards and risks in Ghana

Stunting is associated with the increased risk of sickness and death, slow motoric development, and the delay of mental growth. Stunting can lead to delays in motoric systems development, whether in normal children or in people with a certain disease. The decreased motor function in stunting children without congenital abnormalities related to the low mechanical capability of triceps muscles due to the slow development of muscle function. This research was conducted to know the difference in motor development of stunting and non-stunting in toddlers in the service area of Sentolo I Public Health Centre (PHC), Kulon Progo. This research uses analytical methods of observational with Cross-Sectional Study design. The subjects of this study are 110 stunting and non-stunting children. The samples were taken with consecutive sampling techniques. Methods of data used questionnaires and direct measurement using the height measuring instruments and Denver II sheets. The analysis applies to the chi-squared test. The results show 71.7% of children with stunting in the suspect category on fine motor development, 60.4% of the children with stunting in the suspect category on gross motor development. The results of the statistical test show the score of p-value 0.016 for children in the suspect category on fine motor development and p-value 0.014 for children in the suspect category on gross motor development. The p-value score is < 0.05, meaning there is a significant difference in motoric development stunting and non-stunting children in the service area of Sentolo I PHC, Kulon Progo.

Food Safety Perceptions and Practices among Smallholder Pork Value Chain Actors in Hung Yen Province, Vietnam

BackgroundArmed conflict is a significant social determinant of child health with nuanced effects. There is a dearth of knowledge on the public health issues facing vulnerable populations in conflict-stricken areas. The objective was to determine the prevalence and determinants of moderate to severe anaemia (MdSA) and severe stunting (SS) in children ≤3 years in conflict-hit Dibanda, Ekona and Muea in the Mount Cameroon area.MethodsHaematological parameters were obtained using an automated haematology analyser while undernutrition indices standard deviation (SD) scores (z- scores), were computed based on the WHO growth reference curves for 649 children in a community based cross-sectional study in 2018. Binomial logistic regression models were used to evaluate the determinants of MdSA and SS against a set of predictor variables.ResultsAnaemia was prevalent in 84.0% (545) of the children with a majority having microcytic anaemia (59.3%). The prevalence of MdSA was 56.1% (364). Educational level of parents/caregiver (P < 0.001) and site (P = 0.043) had a significant negative effect on the occurrence of MdSA. Stunting, underweight and wasting occurred in 31.3, 13.1 and 6.3% of the children, respectively. Overall, SS was prevalent in 17.1% (111) of the children. The age groups (0.1–1.0 year, P = 0.042 and 1.1–2.0 years, P = 0.008), educational levels (no formal education, P < 0.001 and primary education P = 0.028) and SS (P = 0.035) were significant determinants of MdSA while MdSA (P = 0.035) was the only significant determinant of SS. On the contrary, age group 0.1–1 year (OR = 0.56, P = 0.043) and site (Dibanda, OR = 0.29, P = 0.001) demonstrated a significant protective effect against SS.ConclusionsModerate to severe anaemia, severe stunting and wasting especially in children not breastfed at all are public health challenges in the conflict-hit area. There is a need for targeted intervention to control anaemia as well as increased awareness of exclusive breast feeding in conflict-hit areas to limit the burden of wasting and stunting.

In 2010 Kenyan authorities reported that 2.3 million bags of corn harvested in that country had been contaminated with fungal poisons known as aflatoxins.1 These toxins—which include aflatoxin B1, the most potent naturally occurring liver carcinogen ever identified—are produced by Aspergillus flavus and A. parasiticus, and they infect corn (maize), nuts, and other crops, especially during periods of drought stress and intense heat. Aflatoxins have been implicated in poisoning outbreaks that killed hundreds of people in developing countries, and experts suspect many aflatoxin-related fatalities go unreported.2 Toxicity risks from aflatoxins are very low in the United States and other developed countries, according to Charles Hurburgh, a professor of agricultural engineering and an extension grain specialist at Iowa State University. People in these countries eat a wide variety of foods with little or no risk of aflatoxin contamination, and for those foods where aflatoxins may occur, contamination is closely monitored and tightly regulated. However, chronic exposures are endemic in developing countries, because aflatoxin monitoring is inadequate, populations tend to rely heavily on just a few staple crops that are vulnerable to Aspergillus infection, and growing conditions often favor mold growth. In a recent analysis of data from the National Health and Nutrition Examination Survey, only 1.3% of more than 2,000 U.S. blood samples had detectible levels of aflatoxins,3 compared with 78% of more than 3,000 blood serum samples from the nationally representative Kenya AIDS Indicator Survey.4 The U.S. Centers for Disease Control and Prevention estimates that 4.5 billion people in the developing world may have chronic exposure to aflatoxins in the diet.5 And according to one analysis, these exposures account for between 25,200 and 155,000 cases of liver cancer every year, particularly in Asia and sub-Saharan Africa.6 Now aflatoxins are drawing international attention from development groups and aid agencies, who are teaching farmers and buyers how to spot and combat the pervasive threat.

Prevalence of tuberculosis infection and its relationship to stunting in children (under five years) household contact with new tuberculosis cases

Stunting continues to be a child public health concern in many African countries, including South Africa. This study uses data from the Birth to Twenty study, held in Johannesburg, to investigate a range of household-level socioeconomic and social support predictors of stunting in children aged less than 30 months. Logistical regression models were constructed using a conceptual framework to investigate the association between early life measures of socio-economic status and stunting (<--2 standard deviations from the WHO (2006) standard), using data collected in the Birth to Twenty study. Stunting prevalence was 18.0% (213/1 186). In unadjusted analyses, numerous socio-economic status exposures showed significant associations with stunting; however, in final multivariable models, decreased likelihood of stunting was seen in children born to mothers who were employed (adjusted odds ratio (AOR) = 0.60, 95% confidence interval (CI) 0.40-0.88), those with fathers who had completed secondary school (AOR = 0.59, 95% CI 0.40-0.85), and whose parents employed a domestic worker (AOR = 0.40, 95% CI 0.19-0.83), while increased likelihood of stunting was seen in male children (AOR = 1.40, 95% CI 1.03-1.91), and those born of low birth weight (AOR = 2.56, 95% CI 1.54-4.26). Stunting and child malnutrition remain policy priorities for the South African Department of Health, and this study suggests that policies that aim to increase parental education level and reduce unemployment or target additional support to families with low education or unemployed parents may reduce stunting in preschool-age children in this setting.

Background: Game meat is consumed in Zambia, yet the supply chain remains weakly regulated compared with that of domestic livestock systems. Wild game, harvested under uncontrolled conditions, often lack veterinary oversight, biosecurity, or hygienic infrastructure, creating food safety risk. In contrast, farmed game benefits from some biosecurity practices, although gaps remain. Understanding these risks is essential for safeguarding public health and promoting sustainable wildlife management. Aim: This study aimed to identify hazardous practices and potential food safety hazards in Zambia’s farmed and wild game meat supply chains and to explore how a One Health (OH) approach, which is an integrative framework that links human, animal, and environmental health, can be applied to manage these risks. Methods: A qualitative mixed-methods design was applied in the Lusaka district, combining 18 key informant interviews, 4 direct observations from local butcheries, and hazard analysis using the Hazard Analysis Critical Control Point (HACCP) framework. The participants included hunters, farmers, butchers, regulators, researchers, conservationists, and consumers. The data were thematically coded using grounded theory, and hazards were then identified from the data using the HACCP framework, with risks ranked by severity and likelihood across sourcing, processing, distribution, sales, consumption and by-products. Findings: Wild game meat poses the greatest food safety risk due to the absence of ante-mortem inspections, unhygienic slaughter and handling in the field, gastrointestinal tract damage during shooting, incomplete bleeding, and transport in open vehicles. Cultural practices such as consuming spoiled meat further increase food safety hazards. Farmed game meat demonstrated lower risks, supported by biosecurity measures, veterinary inspections, and cold storage. However, hazards persist, particularly from broken cold chains and delayed evisceration. Conclusions: Wild game meat consistently presents greater food safety hazards than farmed game meat does, although both require improved oversight. This article shows how an OH approach that integrates veterinary, public health, and environmental (processing and handling) could support the management of food safety risks. The recommended measures include standardized inspections, stronger biosecurity measures, mobile hygienic processing units, cold chain enforcement, consumer education, and regulatory reform. Interdisciplinary collaboration is critical for safer game meat supply chains in Zambia. One Health impact statement This article demonstrates how an OH approach can effectively manage food safety risks in Zambia’s game meat supply chain, benefiting public health, animal welfare, and the environment. By fostering collaboration among the human health, veterinary, environmental, and regulatory sectors, this study identified unsafe food handling and processing practices, associated hazards, and developed targeted interventions that are not possible through isolated efforts. The integration of academic research with practical knowledge from local butchers, game farmers, and government officials enabled the co-production of actionable, context-specific solutions such as improved traceability and biosecurity practices that enhance food safety and reduce disease transmission from game animals to humans through meat handling and consumption. This transdisciplinary strategy has a greater impact by safeguarding both urban consumers and rural livelihoods, supporting sustainable wildlife management, and informing policies for safer, more resilient food systems.

The American Association for Cancer Research has been the citadel for communicating research on chemical carcinogens for over a century. It therefore seems appropriate that a review of chemical carcinogenesis inaugurates a series of articles highlighting advances in understanding, treating, and preventing cancer.At the dawn of the 20th century, we had recognized that chemicals cause cancer, but we had not yet identified individual cancer-causing molecules, nor did we know their cellular targets. We clearly understood that carcinogenesis, at the cellular level, was predominantly an irreversible process. What we lacked was knowledge of the mechanisms by which chemicals cause cancer and the molecular changes that characterize tumor progression.We now are early in a century in which cancer is being investigated at the molecular level, and we have developed technologies that afford unprecedented power to delineate and manipulate altered pathways in cancer cells. Can we harness new insights and technologies to prevent or obliterate human cancers or delay their progression? Can we identify individuals who have a particularly high susceptibility to specific environmental carcinogens?The history of chemical carcinogenesis is punctuated by key epidemiologic observations and animal experiments that identified cancer-causing chemicals and that led to increasingly insightful experiments to establish molecular mechanisms and to reduction of human exposure. In 1914, Boveri (1) made key observations of chromosomal changes, including aneuploidy. His analysis of mitosis in frog cells and his extrapolation to human cancer is an early example of a basic research finding generating an important hypothesis (the somatic mutation hypothesis). The first experimental induction of cancer in rabbits exposed to coal tar was performed in Japan by Yamagiwa and Ichikawa (2) and was a confirmation of Pott's epidemiologic observation of scrotal cancer in chimney sweeps in the previous century (Fig. 1; ref. 3). Because coal tar is a complex mixture of chemicals, a search for specific chemical carcinogens was undertaken. British chemists, including Kennaway (4), took on this challenge and identified polycyclic aromatic hydrocarbons, for example, benzopryene, which was shown to be carcinogenic in mouse skin by Cook, Hewett, and Hieger in 1933 (5). The fact that benzopyrene and many other carcinogens were polyaromatic hydrocarbons lead the Millers (6) to postulate and verify that many chemical carcinogens required activation to electrophiles to form covalent adducts with cellular macromolecules. This in turn prompted Conney and the Millers (7) to identify microsomal enzymes (P450s) that activated many drugs and chemical carcinogens.The discovery of DNA as the genetic material by Avery, MacLeod, and McCarthy (8) and the description of the structure of DNA by Watson and Crick (9) indicated that DNA was the cellular target for activated chemical carcinogens and that mutations were key to understanding mechanisms of cancer. This led to defining the structure of the principal adducts in DNA by benzo(a)pyrene (10) and aflatoxin B1 (11). The concepts developed in investigating mechanisms of chemical carcinogenesis also led to discoveries that are relevant to other human conditions in addition to cancer, including atherosclerosis, cirrhosis, and aging.Global epidemiologic studies have indentified environmental and occupational chemicals as potential carcinogens. The most definitive epidemiologic studies have been those in which a small group is exposed to an inordinately large amount of a specific chemical, such as aniline dyes.Figure 1 illustrates exposure of individuals to residues from fossil fuel in chimneys, to tobacco smoke, and to fungi containing aflatoxin, and the identification of the responsible carcinogen(s). Active smoking and exposure to second-hand smoke are among the major causes of cancer mortality worldwide. Even after causative chemicals are identified, however, measurement of accumulated exposure of individuals in different environments remains an important challenge.The fact that genetic changes in individual cancer cells are essentially irreversible and that malignant changes are transmitted from one generation of cells to another strongly points to DNA as the critical cellular target modified by tobacco smoke and environmental chemicals. DNA damage by chemicals occurs randomly; the phenotypes of associated carcinogenic changes are determined by selection.Cancers caused by environmental agents frequently occur in tissues with the greatest surface exposure to the agents: lung, gastrointestinal tract, and skin. Recently, the study of chemical carcinogenesis has merged with studies on the molecular changes in cancer cells, thus generating biological markers to assess altered metabolic pathways and providing new targets for therapy. Although these are exciting areas, they may be peripheral to attacking the primary causes of the most common human cancers. As we catalog more and more mutations in cancer cells and more and more changes in transcription regulation, it becomes increasingly apparent that we need to understand what generates these changes. The fact that chemicals cause random changes in our genome immediately implies that our efforts need to be directed to quantifying these changes, reducing exposure, and developing approaches to chemoprevention.Chemical carcinogens cause genetic and epigenetic alterations in susceptible cells imparting a selective growth advantage; these cells can undergo clonal expansion, become genomically unstable, and become transformed into neoplastic cells. This classic view of carcinogenesis has its origin in experimental animal studies conducted in the mid 20th century. The first stage of carcinogenesis, tumor initiation, involves exposure of normal cells to chemical or physical carcinogens. These carcinogens cause genetic damage to DNA and other cellular macromolecules that provide initiated cells with both an altered responsiveness to their microenvironment and a proliferative advantage relative to the surrounding normal cells.Early in the field of chemical carcinogenesis, investigators recognized that perturbation of the normal microenvironment by physical means, such as wounding of mouse skin or partial hepatectomy in rodents (12, 13) or chemical agents, such as exposure of the mouse skin to certain phorbol esters (14), can drive clonal expansion of the initiated cells toward cancer. In the second stage, tumor promotion results in proliferation of the initiated cells to a greater extent than normal cells and enhances the probability of additional genetic damage, including endogenous mutations that accumulate in the expanding population. This classic view of two-stage carcinogenesis (14) has been conceptually important but also an oversimplification of our increasing understanding of the multiplicity of biological processes that are deregulated in cancer. In addition, an active debate continues on the relative contribution of procarcinogenic endogenous mechanisms—for example, free-radical–induced DNA damage (15), DNA depurination (16), DNA polymerase infidelity (17), and deamination of 5-methylycytosine (18)—compared with exposure to exogenous environmental carcinogens (19). The enhancement of carcinogens by epigenetic mechanisms such as halogenated organic chemicals and phytoestrogens (20), as well as the extrapolation of results from animal bioassays for identifying carcinogens to human cancer risk assessment, are also difficult to quantify (21). As discussed below, this debate is not merely an academic one, in that societal and regulatory decisions critical to public health are at issue. The identification of chemical carcinogens in the environment and occupational settings [benzo(a)pyrene and tobacco-specific nitrosamines in cigarette smoke, aflatoxin B1 (AFB1) residues from fossil fuel, vinyl chloride, and benzene] has led to regulations that have reduced the incidence of cancer.A timeline of selected experimental advances in chemical carcinogenesis that have important implications is presented in Fig. 2. First, the selected advances reflect the judgment of the authors and consultants, and remain to be modified by the readers, and, ultimately, by history. Second, the timeline shows the progression of results; an important observation generates new hypotheses that are tested by experiments with increasing mechanistic focus. Third, the timeline is punctuated with three important molecular discoveries (DNA structure, DNA sequence, and the PCR) that refocused experiments in chemical carcinogenesis (9, 22, 23). Fourth, many technological advances have allowed conceptual ideas to be experimentally tested, including the sensitive detection of chemical carcinogens by high-pressure liquid chromatography (24) and mass spectrometry (25), detection of DNA adducts by postlabeling (26) and by specific antibodies (27), transcriptional profiling by arrays (28, 29), and quantitation of mutagenicity of carcinogens using bacterial genetics (19).In the first half of the 20th century, the experimental focus was on identifying chemical carcinogens in complex mixtures, and on determining their metabolism and cellular targets. With the recognition that genes are encoded in DNA (9) and that DNA is transferred from one cellular generation to the next (30), research rapidly focused on the interaction of activated chemical carcinogens with DNA and on mutations that result from DNA alterations as well as the identification of key mutated (31) or deregulated genes including oncogenes and tumor suppressor genes (32). Underlying these studies was the expectation that delineation of mutated genes would identify them as specific targets for chemotherapy. The expectation that targeting individual mutated or rearranged gene products would be efficacious for cancer treatment has thus far been verified in only a limited number of situations, such as the use of imatinib for chronic myelogenous leukemia (33).The experimental landmarks highlighted in Fig. 2 frequently generated new experiments, and this progression has foretold some of our key concepts on the mechanisms of chemical carcinogenesis. An overriding concept has emerged that links DNA damage by reactive chemicals, the production of mutations by unrepaired DNA adducts, and the selection of cells harboring mutated genes that characterize the malignant phenotype. Studies on arylhydroxylamines provided a paradigm for tracing the metabolism of carcinogens to chemically reactive electrophiles that covalently bind to DNA. 2-Acetylaminofluorene (AAF) is metabolically activated by liver microsomal mixed–function oxygenases to N-hydroxy- and then to N-sulf oxy-AAF, a strong electrophile that forms covalent adducts with guanine moieties in DNA (34). AAF is not mutagenic in bacterial assays, whereas N-hydroxy-AAF is highly carcinogenic (34). N-hydroxy-AAF is rendered inactive by the formation of a glucuronide in the liver that is transported to the bladder and excreted (35). Unfortunately, it is subjected to acid hydrolysis in the bladder to yield active N-hydroxy-AAF, which is associated with human bladder cancer. Thus, the activation and detoxification of a chemical carcinogen in specific cells or tissues can be a major factor in determining tissue and host specificity.The testing of certain concepts in chemical carcinogenesis awaited the development of new technologies. For example, the concept of somatic mutations in cancer (1, 36) preceded by 40 years the establishment of DNA as the genetic material (8) and by 63 years the development of DNA sequencing methods (23) that directly showed clonal mutations in human cancer cells. Also, the mutator phenotype hypothesis formulated in 1974 (17) has been only recently experimentally verified (37).Many hypotheses are still under active investigation. These include the potential importance of carcinogen-protein interactions (38), carcinogen-induced reversion to stem cell–like phenotypes (39), inherited changes in gene expression (40, 41), direct action of nongenotoxic chemicals (42), and targeted interactions of carcinogens with specific genes such as TP53 (43–45). Other concepts focus on carcinogenesis mediated by RNA damage (46), RNA-templated DNA repair (47), specific metastasis genes (48, 49), and sequential clonal lineage pathways in cancer (50, 51).Emerging hypothesis such as anticarcinogens (52), overlapping pathways to malignancy (53), coordinated changes in gene expression (54), epigenetic silencing by chemical carcinogens (40, 55, 56), and oncogene addiction (57) are just beginning to be explored. Finally, there are concepts for which quantitation is lacking, yet have stood the test of time based on their inherent significance; these include the importance of anaerobic metabolism by tumors (58, 59) and the initiation of tumorigenesis by the generation of oxygen-reactive species (15).Although establishing DNA as the genetic material provided a structure that faithfully can be duplicated during each cell division, it rapidly became apparent that DNA was also subject to direct modification by X-rays (60), alkylating agents (61), and by an increasing number of environmental chemicals (62, 63). Changes in DNA by many chemical carcinogens are indirect; they first require activation by P-450 aryl hydroxylases into electrophiles to form covalent adducts with DNA and with other cellular macromolecules (64, 65). Many normally generated reactive molecules that are intermediates in metabolism modify many cellular molecules including DNA and therefore are mutagens and carcinogens. However, not all mutagens seem to be carcinogens. What was unanticipated was the magnitude of DNA modification by normal cellular processes in the absence of exposure to environmental mutagens (66, 67).The lability of DNA in an aqueous environment was first quantified by Lindahl and Nyberg, who measured the rates of depurination (16) and deamination (18) in solution under different conditions and extrapolated these results to those predicted to be present in human cells. They calculated that each normal cell could undergo >10,000 DNA damaging events per day. Endogenously generated modifications of DNA include methylation by S-adenosylmethione, modification by lipid peroxidation products, chlorination, glycosylation, oxidation, and nitrosylation (66–71). Reactive oxygen and nitrogen species are particularly relevant because the activated species are generated by host cells, and the process of resynthesis results in the replacement of >50,000 nucleotides per cell per day (68). To maintain our genomes, we have evolved a network of DNA repair pathways to excise altered residues from DNA (Fig. 3). A major consideration is the relative contribution of environmental and endogenous DNA damage to carcinogenesis. DNA damage by environmental agents would have to be extensive and exceed that produced by normal endogenous reactive chemicals to be a major contributor to mutations and cancer. This consideration underlines the difficulty in extrapolating risk of exposure to that which would occur at very low doses of carcinogens.Human cells possess an armamentarium of mechanisms for DNA repair that counter the extensiveness of DNA damage caused both by endogenous and environmental chemicals. These mechanisms include base excision repair (BER) that removes products of alkylation and oxidation (72–74); nucleotide excision repair (NER) that excises oligonucleotide segments containing larger adducts (75); mismatch repair that scans DNA immediately after polymerization for misincorporation by DNA polymerases (76); and oxidative demethylation (77), transcription-coupled repair (TCR) that preferentially repairs lesions that block transcription (78); double-strand break repair and recombination that avoids errors by copying the opposite DNA strand (79); as well as mechanisms for the repair of cross-links between strands (80, 81) that yet need to be established.Most DNA lesions are subject to repair by more than one pathway. As a result, only a minute fraction of DNA lesions escapes correction are present at the time of DNA replication and can direct the incorporation of noncomplementary nucleotides resulting in mutation (Fig. 3). Unrepaired DNA lesions initiate mutagenesis by stalling DNA replication forks or are copied over by error-prone trans-lesion DNA polymerases (82–84). Alternatively, incomplete DNA repair can result in the accumulation of mutations and mutagenic lesions, such as abasic sites (85).Damage to DNA by chemical carcinogens activates checkpoint signaling pathways leading to cell cycle arrest and allows time for DNA repair processes. In the absence of repair, cells can use special DNA polymerases that copy past DNA adducts (86, 87), or undergo apoptosis by signaling the recruitment of immunologic and inflammatory host defense mechanisms. The demonstration that each methylcholanthrene-induced tumor has a unique antigenic signature provided one of the earliest glimpses into the stochastic nature of cellular responses to carcinogens (88). The immunologic and inflammatory responses facilitate not only engulfment and clearance of damaged cells but also the resulting generation of reactive oxygen (89) and nitrogen radicals (90) that further damage cellular DNA.The concept that chronic inflammation can result in cancer is supported by Virchow's (91) histologic observation of inflammatory lymphocytes infiltrating tumors. Inflammation accompanying the "painting" of coal tar was described by Japanese pathologists in the earliest experimental study of chemical carcinogenesis (2). The classic tumor promoter, croton oil, and its most active ingredient, 12-O-tetradecanoylphorbol-13-acetate, are potent inflammatory agents. In addition to studies of "two-stage" skin carcinogenesis, other animal models have shown the synergistic interaction of chemical carcinogens with proinflammatory agents; for example, respiratory infection with influenza virus synergistically increases the lung cancer response in rats to a carcinogenic N-nitrosamine (92).Chronic inflammation can have a strong inherited basis, e.g. hemochromatosis, or can be acquired from infection by viruses, bacteria, or parasites or be associated with metabolic or physical conditions (93). Obesity has been considered to be a chronic inflammatory condition associated with multiple types of human cancer (94); gastric acid reflux causes chronic inflammation and can progress to Barrett's-associated esophageal adenocarcinoma (95); and colitis can progress to colon cancer (96, 97). Recent advances have begun to uncover the underlying mechanisms of the association between chronic inflammation and cancer.The identification of specific genes by allelic replacements and "knockouts" has facilitated the delineation of complex immune response networks that govern cellular responses to chemical carcinogens. The innate immune system is the first line of defense against pathogenic microorganisms and toxins and responds by generating free radicals, inflammatory cytokines, and the activation of the complement cascade (93, 98). In addition to reactive oxygen species, the past two decades have shown the significance of nitrogen-based free radicals, including nitric oxide and its derivatives (90, 93). The concentration and length of exposure can determine the seemingly paradoxical procarcinogenic and anticarcinogenic activities of free As be discussed in another in the chronic activation of the innate immune system is procarcinogenic and immune system is anticarcinogenic there is a to from an individual is exposed to a carcinogen to the detection of a For most there is an in cancer incidence as a of that tumor progression in a series of sequential This process has been most in colon cancer, with the progression from to to and to metastasis of cancers at different from to a sequential of mutations and genome mutations in DNA activation of of on and of This concept of sequential mutations has been by new including the of somatic mutations in and colon cancers and the demonstration that only a small fraction of colon cancers the three most frequently identified mutations this may identify potential not cancers a mutator a more stochastic cancer cell in a tumor of different and yet only a small of cells preferentially during to random mutations that a selective advantage for this concept is the demonstration that the of mutations in human cancers is greater than that in normal tissues in cell and adenocarcinoma of the colon The genetic of cancer cells produced by mutator mutations increases the that a tumor many cells to and is with the of of research in chemical carcinogenesis have provided a for the analysis of adducts and somatic mutations in as of carcinogen exposure. A paradigm for between of carcinogens exposure and a cancer risk is shown in Fig. a is a example of an environmental chemical carcinogen that has been using this a polycyclic aromatic (53), an aromatic and a tobacco-specific N-nitrosamine are other key epidemiologic studies a association between exposure and the incidence of studies of in multiple animal species, chemical and analysis of the identification of DNA adducts, and of mutagenic the for and to as a human carcinogen from these experimental animal and studies were then and to assess exposure and biological in studies conducted in of high exposure and high incidence of such as and The were and to the of the that is a human The between and was further by the association between exposure and a specific mutation in the nucleotide of of the tumor suppressor gene in In from and The a synergistic interaction between exposure or and of virus infection in the risk of was remain to be For example, the molecular of the synergistic interaction between and is still the and oxidative of to the gene incorporation in the genome of their of by advances in molecular are and they increasingly are being to understanding the interaction of chemical carcinogens with cellular and of DNA has facilitated the identification of specific genes mutated in human cancers. including mass to carcinogen with unprecedented and spectrometry is being with mutagenesis to specific alterations in DNA of the human genome and the identification of DNA enzymes the field of molecular in on individual susceptibility to carcinogens. analysis of carcinogen-induced alterations in the expression of both and the are that can molecules of carcinogens in cells, random mutations in individual cells, analysis of the of molecules and and and genetic to delineate complex pathways in cells. Underlying this progress in understanding chemical carcinogenesis is a cascade of advances in molecular that it to quantify DNA damage by chemical agents, and changes in gene the structure of DNA and the cell including carcinogenesis. in detection of DNA damage, including postlabeling of DNA (27), and mass spectrometry (25), have allowed the detection of a altered base in nucleotides using human DNA. This can be to DNA or RNA in a cell in cell including and it to assess changes in RNA and expression during carcinogenesis. these technologies it increasingly to pathways in cancer cells from to to to have made in identifying chemical carcinogens and their mechanisms of We have increasingly focused on DNA as a the fact at the cellular level, cancer is an inherited a cancer, a cancer. The efforts to chemicals as potential or human carcinogens are not but in most are in The need to identify chemical carcinogens in of human exposure and epidemiologic is on mechanistic and knowledge of and among animal species is a For example, the of in the by a not to be relevant to carcinogenesis, is initiated by epidemiologic verified by animal experiments, and by mechanistic and studies The between carcinogen exposure and the induction of cancer continues to be a of and public debate The of a is a in the of public health that to be as mechanistic accumulate in the field of chemical carcinogenesis has a history of that of cancer cancer risk assessment, public health and and occupational causes of cancer. The concepts of interactions and in the molecular of human cancer risk were generated by the of chemical carcinogenesis, cellular and molecular and cancer genetic in DNA repair and enzymes are of an inherited of in cancer susceptibility of the of cancer risk and detection are based on the knowledge of chemical carcinogenesis, including adducts, somatic and mutation carcinogen exposure and DNA with interactions can have synergistic for example, and in carcinogenesis. models of chemical carcinogenesis to a critical in the field of cancer and in our understanding the mechanisms of cancer and the of in in the field of chemical carcinogenesis remain to be stem cells mutated by chemical carcinogens and become of human chemical carcinogens epigenetic changes during These and other many to be formulated by to investigators in chemical carcinogenesis our understanding of carcinogenesis, and, as a result, cancer and potential of were Cancer and and by The Research of the Cancer for Cancer Research of of this were in by the of This therefore be in with to this selection of the major events in this review of the field are the primary of the with the of the The authors for many of which are of importance to the field of chemical carcinogenesis. We on this subject We for Fig. of chimney and for Fig. and of smoking and aflatoxin, and and for their critical

An Economic Evaluation of PulseNet: A Network for Foodborne Disease Surveillance.

Human helminthiasis, particularly soil-transmitted helminth (STH) infections, is a prevalent health concern in Indonesia, especially among children, often resulting in growth disorders, notably stunting. To examine the link between STH infections and childhood stunting, we conducted a comprehensive review of literature spanning 2012-2023, encompassing 40 selected articles from databases like PubMed, Science Direct, and Google Scholar. Our analysis revealed a substantial association between STH infections and increased stunting risk in children, estimating a 44.407% rise in stunting risk due to STH infection. Stunting, a consequence of chronic malnutrition, profoundly affects a child's physical and cognitive development, with long-lasting repercussions on their future potential and quality of life. This study has significant implications. It underscores the urgent need for robust public health interventions targeting STH infections, especially in high-prevalence areas like Indonesia. Measures such as mass deworming campaigns, improved sanitation and hygiene practices, and health education can significantly alleviate the burden of STH infections and the resulting stunting. Moreover, the research emphasizes the intricate relationship between infectious diseases and malnutrition, highlighting the necessity for a holistic approach to child health. Addressing STH infections necessitates not only medical intervention but also efforts to enhance overall living conditions and nutritional status. Integrating these approaches into a comprehensive public health strategy can yield more effective and sustainable results in the fight against childhood stunting. In conclusion, this study underscores the paramount importance of addressing STH infections in the context of child growth and underscores the urgency of implementing effective public health interventions. This approach can enable children to reach their full physical and cognitive potential, ultimately contributing to the overall well-being and development of societies.

Back to table of contents Previous article Next article Health Care EconomicsFull AccessPublic Health Shifts Focus To Preventing Chronic IllnessMark MoranMark MoranSearch for more papers by this authorPublished Online:1 Dec 2006https://doi.org/10.1176/pn.41.23.0015American public health, long focused on control of infectious disease, is undergoing a fundamental change in outlook as it turns its attention to chronic disease, including mental illness.So said psychiatrist Neil Cohen, M.D., New York City's former commissioner of health, during a lecture on public health challenges in psychiatry at the APA institute on Psychiatric Services in New York in October.Cohen said the success of American public health measures over the last 100 years in controlling infectious disease, combined with the increase in prevalence of chronic conditions, is forcing a change in the priorities of public health departments across the country. And with this change has come a recognition of the pervasiveness of mental illness.Meanwhile, psychiatric epidemiology research has advanced to the point that risk factors can be identified. “Psychiatric epidemiology is not just about counting anymore,” Cohen said. “We are at the dawn of an era when we can now look at risk-factor epidemiology, examining the causes that contribute to—and the protective factors that decrease risks for—mental illness in communities.“The knowledge to be gained from modern-day psychiatric epidemiology is as much about psychopathology and understanding the roots of mental illness as it is about epidemiology,” he said. “The advances that derive from this approach allow us to look at subthreshold syndromes, at the number of factors at play that put an individual at risk for advancing pathology.”Cohen was the city's health commissioner from 1998 to 2002. In that post, he oversaw the public health responses to several crises: the outbreak of West Nile virus, the attacks on the World Trade Center, and anthrax-laced letters sent to media outlets in the city. He also served as commissioner of the New York Department of Mental Health, Mental Retardation, and Alcoholism Services, and he oversaw the merger of the health and mental health departments into a unified public health agency. He is currently clinical director and vice chair of the department of Psychiatry at mt. Sinai Medical Center and director of its Division of Community Medicine.Infectious-Disease Focus Has a PriceCohen noted that the significant extension of life expectancy for Americans during the 20th century was due not so much to medical advances as to the success of core public health activities such as improvements in nutrition and hygiene and the monitoring and control of infectious diseases.“But the preoccupation with infectious disease came with a cost,” Cohen said. “it slowed the development of measures to deal with stroke, heart disease, and diabetes. And it limited the amount of attention that was paid to curtailing high-risk behaviors that contribute to prevalence of chronic conditions.”The focus began to shift in the early 1990s, with the emergence of several lines of research demonstrating the profound effect of behavior on human health.“Despite the need for public health interventions to address behavior, only 5 percent of each health care dollar is devoted to behavior modification,” Cohen stated.Related to this have been the historic neglect of mental health and illness and the segregation of public mental health activities from the rest of public health and medicine. These too have begun to change in the wake of studies in the early 1990s by the World Bank and Harvard School of Public Health showing the enormous burden of disease related to mental illness.That research found that major depression trailed behind only ischemic heart disease in terms of lost years of productivity due to death or disability and that depressive disorders, taken together, are the leading cause of disability worldwide.Satcher Reports Changed ThinkingEven more powerful were the reports on mental health and illness by former Surgeon General David Satcher, M.D. Along with President Bush's New Freedom Commission on Mental Health and the enormous strides made in biomedical research on mental illness, the result has been a slow but certain realignment of priorities.Cohen said the threat of terrorism and bioterrorism has also galvanized the integration of mental health and public health. Drawing on his experience helping to coordinate the response to the terrorist attacks on September 11, 2001, Cohen said there has been an effort to “bring mental health issues to bear on the larger public health response” to the threat of terrorism and bioterrorism.And those threats have raised the profile of public health departments.“ In this post-9/11 world, the decades-long neglect of the public health system has been changing,” Cohen said. “Increasingly, the public and government are aware that a robust public health infrastructure is critical to the capacity to respond to a whole host of emerging threats.”Cohen believes that a principal public health challenge facing psychiatry today is to draw on the new power of psychiatric epidemiology to develop models that focus on maintenance of positive mental health and prevention of mental illness rather than merely the treatment of disease when it appears. And he cited satcher in pointing out that “successful performance really rests on a foundation of successful mental health.”Neil Cohen, M.D.: “Increasingly, the public and government are aware that a robust public health infrastructure is critical to the capacity to respond to a whole host of emerging threats.” Ellen Dallager“What I've been talking about is an alignment with the larger public health system and a greater focus on community well-being than has heretofore been our focus,” Cohen said. “The relationship between physical and mental disorders is profoundly influential with respect to morbidity and mortality and could very well be the core of a new model of public mental health...[that will] really take up the challenge of improving quality of life not only for individuals but entire communities.” ▪ ISSUES NewArchived

Background: Stunting in children is often associated with infectious diseases, one of which is Soil Transmitted Helminths (STH). Worms in child­ren affect the intake, digestion, absorption and metabolism of food which has an impact on reducing the supply of nutrients to the body. This study aimed to determine the relationship between STH and the incidence of stunting in children aged 6-12 years in Pinrang, South Sulawesi. Subjects and Method: This was an analytic observational with cross sectional design. The study was conducted in Pinrang Regency, South Sulawesi, from January to March 2020. A sam­ple of 200 children aged 6-12 years was selected by random sampling. The dependent variable was stunting. The independent variables were worm disease, maternal education, family income, number of family members, maternal body height, low birth weight, length of birth, exclusive breastfeeding, and complementary feed­ing. The data were collected by question­naire and analyzed by a multiple multilevel logistic regression run on STATA13. Results: The risk of stunting increased with worms (b= 2.11; 95% CI= 1.11 to 3.10; p <0.001), low maternal education (b= 1.08; 95% CI= 0.13 to 2.03; p= 0.025), low income (b= 1.03; 95% CI= 0.05 to 2.02; p= 0.039), number of family (b= 2.13; 95% CI= 1.13 to 3.13; p< 0.001), short maternal height (b= 1.03; 95% CI= 0.10 to 1.96; p= 0.030), LBW (b= 1.45; 95% CI= 0.38 to 2.51; p= 0.007), short birth length (b= 1.91; 95% CI= 0.95 to 2.87; p< 0.001), and inappropriate complementary feed­ing (b= 1.11; 95% CI= 0.21 to 2.11; p= 0.029). The risk of stunting decreased with exclusive breastfeeding (b= 0.96; 95% CI= 0.23 to 1.91; p= 0.045). Village had negligible contextual effect on the stunting with ICC= 8.2%. Conclusion: The risk of stunting increases with worms, low maternal education, low income, number of family, short maternal height, LBW, short birth length, and inappro­priate complementary feed­ing. The risk of stun­ting decreases with exclusive breastfeed­ing. Village has negligible contextual effect on the stunting. Keyword s : stunting, soil transmitted helminths Correspondence: Putri Andini Muslimah. Masters Program in Public Health, Universitas Sebelas Maret, Jl. Ir. Sutami 36A, Surakarta 57126, Central Java. Email: ptriandn15@gmail.com. Mobile: +6285­331663133. Journal of Epidemiology and Public Health (2020), 05(03): 372-383 https://doi.org/10.26911/jepublichealth.2020.05.03.11.

Regional Character, Restaurant Size, and Food Safety Risk: Evidence from Food Safety Violation Data in Gansu Province, China