• Safety and Health at Work
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• 제3권2호
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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.

• 한국식품영양과학회:학술대회논문집
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• 한국식품영양과학회 2004년도 Annual Meeting and International Symposium
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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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• 제13권6호
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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.

• 한국환경성돌연변이발암원학회:학술대회논문집
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• 한국환경성돌연변이발암원학회 2001년도 Korean Environmental Mutagen Society
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• pp.17-18
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• 2001

• Journal of Preventive Medicine and Public Health
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• 제42권6호
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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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• 제16권3호
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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.

• 고려인삼학회:학술대회논문집
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• 고려인삼학회 2003년도 춘계 총회 및 학술대회
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• pp.50-51
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• 2003

• Journal of Preventive Medicine and Public Health
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• 제49권2호
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• pp.80-96
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• 2016

최근 담배제조회사의 불법행위법상 손해배상책임을 둘러싼 소송이 계속되고 있다. 이미 대법원 판결이 나온 사건도 있고, 현재 소송이 계속 중인 사건도 있는데, 원고가 증거로 제출한 역학 자료에 의하여 흡연과 질병 사이의 인과관계가 증명되었다고 볼 수 있는지가 이 사건들의 공통된 주요 쟁점이다. 담배소송에서 인과관계의 증명이 쟁점으로 부각되는 까닭은 흡연에 따른 질병의 발생이 흡연 외의 다양한 요인의 영향을 받을 뿐만 아니라 흡연과 발병 사이의 시간적 간격도 길어 원고가 인과관계의 증명에 곤란을 겪기 때문이다. 흡연자 담배소송의 대법원 판결(대판 2014. 4. 10, 2011다22092)은 역학적 증거에 의한 인과관계의 증명 여부에 관하여 비교적 신중한 입장을 취하고 있는데, 몇 가지 아쉬움이 남는다. 첫째, 대법원은 질병을 특이성 질환과 비특이성 질환으로 2분하여 양자 사이에 인과관계의 증명방법을 달리 보았다. 그러나 특이성 질환의 개념은 발병요인에 관하여 의학계와 보건학계에서 확립된 학설인 다요인설에 배치된다. 더구나 불법행위법의 영역에서 특이성 질환 개념을 새로 도입하여야 할 필요성도 발견하기 어렵다. 둘째, 대법원은 비특이성 질환의 경우에 역학적 상관관계가 인정된다고 하더라도 원고가 위험인자에 노출된 시기와 노출 정도, 발병시기, 그 위험인자에 노출되기 전의 건강상태, 생활습관 등을 증명하여 그 위험인자에 의하여 비특이성 질환이 유발되었을 개연성을 증명하여야 한다고 하였다. 하지만 질병과 위험인자와의 역학적 관련성이 상당한 강도에 이른 경우에도 여전히 원고에게 추가적 증명책임을 부과하는 것은 권리구제의 범위를 지나치게 좁힐 우려가 있다. 셋째, 대법원이 이처럼 역학적 증거의 가치를 인정하는 데에 소극적인 까닭은 역학적 연구가 개인이 아닌 특정인구집단을 대상으로 한 것이기 때문으로 보인다. 그러나 역학적 증거가 집단의 구성원인 개인(들)에 대하여 가치 있는 정보를 제공하지 못한다고 단정하기에는 이르다. 예컨대, 역학에서 산출하는 인과확률은 집단 내에서 무작위로 뽑아낸 환자의 질병 발생이 위험인자에 의해 발생하였을 확률을 나타내는데, 이는 집단 차원의 확률을 구성원인 개인의 확률로 전환하는 유용한 지표이므로 역학적 증거만으로도 인과관계의 개연성을 증명할 여지가 있다고 생각된다.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 추계학술대회
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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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• 제4권3호
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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.