• Safety and Health at Work
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• v.3 no.2
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• pp.110-116
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• 2012

Establishing a causal relationship between factors at work and disease is difficult for occupational physicians and researchers. This paper seeks to provide arguments for the judgement of evidence of causality in observational studies that relate work factors to disease. I derived criteria for the judgement of evidence of causality from the following sources: the criteria list of Hill, the approach by Rothman, the methods used by International Agency for Research on Cancer (IARC), and methods used by epidemiologists. The criteria are applied to two cases of putative occupational diseases; breast cancer caused by shift work and aerotoxic syndrome. Only three of the Hill criteria can be applied to an actual study. Rothman stresses the importance of confounding and alternative explanations than the putative cause. IARC closely follows Hill, but they also incorporate other than epidemiological evidence. Applied to shift work and breast cancer, these results have found moderate evidence for a causal relationship, but applied to the aerotoxic syndrome, there is an absence of evidence of causality. There are no ready to use algorithms for judgement of evidence of causality. Criteria from different sources lead to similar results and can make a conclusion of causality more or less likely.

• Proceedings of the Korean Society of Food Science and Nutrition Conference
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• 2004.11a
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• pp.24-36
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• 2004

Polyphenolic flavonoids are among a wide variety of phytochemicals present in the human diet. Basic research, animal model, and human studies suggest flavonoid intake may reduce the risk of several age-related chronic diseases. The vast number of flavonoids and mixtures of their subclasses, including flavonols, flavones and flavanones, and the variety of agricultural practices that affect their concentration in foods have presented a challenge to the development of adequate food composition databases for these com-pounds. Nonetheless, dietary assessments have been applied to cohort and case-control epidemiological studies and several reveal an inverse association with risk of some forms of cancer, cardiovascular disease, and other chronic conditions. Those observational studies that have examined these relationships with regard to flavonols, flavones, and flavanones are reviewed. The requirement for caution in interpreting these studies is discussed with regard to the limited information available on the bioavailability and biotransformation of these flavonoids. As the totality of the available evidence on these flavonoids suggests a role in the prevention of cancer and cardiovascular disease, further research is warranted, particularly in controlled clinical trials.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.6
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• pp.2429-2435
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• 2012

Methyl isocyanate may have a role in cancer etiology, although the link is unclear. There is evidence in the literature that it can induce cancer in animals but the carcinogenic potency is weak. Pheochromocytoma of adrenal medulla and acinar cell tumors of pancreas have been observed in methyl isocyanate exposed animals. Conversely, emerging data from population-based epidemiological studies are contradictory since there is no evidence of such cancers in methyl isocyanate exposed humans. Recently, we reported a high prevalence of breast and lung cancers in such a population in Bhopal. In vitro findings appearing in the latest scientific literature suggest that genomic instability is caused by methyl isocyanate analogs in lung, colon, kidney, ovary epithelial cells, and that hepatocytes may undergo oncogenic transformation, have obvious implications. The conflicting information prompted us to present this update over the last three decades on methyl isocyanate-induced cancers after an extensive literature search using PubMed. While the pertinent literature remains limited, with a scarcity of strong laboratory analyses and field-epidemiological investigations, our succinct review of animal and human epidemiological data including in vitro evidences, should hopefully provide more insight to researchers, toxicologists, and public health professionals concerned with validation of the carcinogenicity of methyl isocyanate in humans.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2001.10b
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• pp.17-18
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• 2001

• Journal of Preventive Medicine and Public Health
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• v.42 no.6
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• pp.360-370
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• 2009

Genetic factors clearly play a role in carcinogenesis, but migrant studies provide unequivocal evidence that environmental factors are critical in defining cancer risk. Therefore, one may expect that the lower availability of substrate for biochemical reactions leads to more genetic changes in enzyme function; for example, most studies have indicated the variant MTHFR genotype 677TT is related to biomarkers, such as homocysteine concentrations or global DNA methylation particularly in a low folate diet. The modification of a phenotype related to a genotype, particularly by dietary habits, could support the notion that some of inconsistencies in findings from molecular epidemiologic studies could be due to differences in the populations studied and unaccounted underlying characteristics mediating the relationship between genetic polymorphisms and the actual phenotypes. Given the evidence that diet can modify cancer risk, gene-diet interactions in cancer etiology would be anticipated. However, much of the evidence in this area comes from observational epidemiology, which limits the causal inference. Thus, the investigation of these interactions is essential to gain a full understanding of the impact of genetic variation on health outcomes. This report reviews current approaches to gene-diet interactions in epidemiological studies. Characteristics of gene and dietary factors are divided into four categories: one carbon metabolism-related gene polymorphisms and dietary factors including folate, vitamin B group and methionines; oxidative stress-related gene polymorphisms and antioxidant nutrients including vegetable and fruit intake; carcinogen-metabolizing gene polymorphisms and meat intake including heterocyclic amins and polycyclic aromatic hydrocarbon; and other gene-diet interactive effect on cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.3
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• pp.1303-1306
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• 2015

Studies of epidemiological and prognostic factors are very important for oncology practice. There is a rapidly increasing amount of research and resultant knowledge in the scientific literature. This means that health professionals have major challenges in accessing relevant information and they increasingly require best available evidence to make their clinical decisions. Meta-analyses of prognostic and other epidemiological factors are very practical statistical approaches to define clinically important parameters. However, they also feature many obstacles in terms of data collection, standardization of results from multiple centers, bias, and commentary for intepretation. In this paper, the obstacles of meta-analysis are briefly reviewed, and potential problems with this statistical method are discussed.

• Proceedings of the Ginseng society Conference
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• 2003.05a
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• pp.50-51
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• 2003

• Journal of Preventive Medicine and Public Health
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• v.49 no.2
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• pp.80-96
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• 2016

Recently, a series of lawsuits were filed in Korea claiming tort liability against tobacco companies. The Supreme Court has already issued decisions in some cases, while others are still pending. The primary issue in these cases is whether the epidemiological evidence submitted by the plaintiffs clearly proves the causal relationship between smoking and disease as required by civil law. Proving causation is difficult in tobacco lawsuits because factors other than smoking are involved in the development of a disease, and also because of the lapse of time between smoking and the manifestation of the disease. The Supreme Court (Supreme Court Decision, 2011Da22092, April 10, 2014) has imposed some limitations on using epidemiological evidence to prove causation in tobacco lawsuits filed by smokers and their family members, but these limitations should be reconsidered. First, the Court stated that a disease can be categorized as specific or non-specific, and for each disease type, causation can be proven by different types of evidence. However, the concept of specific diseases is not compatible with multifactor theory, which is generally accepted in the field of public health. Second, when the epidemiological association between the disease and the risk factor is proven to be significant, imposing additional burdens of proof on the plaintiff may considerably limit the plaintiff's right to recovery, but the Court required the plaintiffs to provide additional information such as health condition and lifestyle. Third, the Supreme Court is not giving greater weight to the evidential value of epidemiological study results because the Court focuses on the fact that these studies were group-level, not individual-level. However, group-level studies could still offer valuable information about individual members of the group, e.g., probability of causation.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.34-63
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• 2003

Idiopathic Parkinson's disease (IPD) represents a common neurodegenerative disorder. While epidemiological studies have suggested a number of risk factors including age, gender, race, and inherited disorder, the cumulative evidence supports the view that environmental or occupational exposure to certain chemicals may contribute to the initiation and progress of Parkinsonism.(omitted)

• Safety and Health at Work
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• v.4 no.3
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• pp.123-135
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• 2013

Exposure to manganese (Mn) is associated with neurobehavioral effects. There is disagreement on whether commonly occurring exposures in welding, ferroalloy, and other industrial processes produce neurologically significant neurobehavioral changes representing parkinsonism. A reviewof methodological issues in the human epidemiological literature onMnidentified: (1) studies focused on idiopathic Parkinson disease without considering manganism, a parkinsonian syndrome; (2) studies with healthy worker effect bias; (3) studies with problematic statistical modeling; and (4) studies arising from case series derived from litigation. Investigations with adequate study design and exposure assessment revealed consistent neurobehavioral effects and attributable subclinical and clinical signs and symptoms of impairment. Twenty-eight studies show an exposure-response relationship between Mn and neurobehavioral effects, including 11 with continuous exposure metrics and six with three or four levels of contrasted exposure. The effects of sustained low-concentration exposures to Mn are consistent with the manifestations of early manganism, i.e., consistent with parkinsonism. This is compelling evidence thatMnis a neurotoxic chemical and there is good evidence that Mn exposures far below the current US standard of $5.0mg/m^3$ are causing impairment.