The Chernobyl Disaster: Cancer following the Accident at the Chernobyl Nuclear Power Plant

Article (PDF Available)inEpidemiologic Reviews 27(1):56-66 · February 2005with102 Reads
DOI: 10.1093/epirev/mxi012 · Source: PubMed

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Available from: Lydia B Zablotska
    • "Thirty years have passed since the Chernobyl accident led to exposure of millions of people in Europe. Studies of populations [33] exposed have provided significant new information on radiation risks, particularly in relation to thyroid tumours following exposure to iodine isotopes. Recent studies among Chernobyl liquidators [42] have also provided evidence of increases in the risk of leukaemia and other haematological malignancies and of cataracts , and suggestions of increases in the risk of cardiovascular diseases, following low doses and low dose rates of radiation. "
    [Show abstract] [Hide abstract] ABSTRACT: Objective: We raised the question of a possible relationship in Belgium between the occurrence of papillary thyroid carcinoma (PTC) and age of children (<15 years) at the time of the Chernobyl nuclear plant accident in April 1986. Setting: Referral university centre for endocrine surgery. Material and methods: Thirty-year prospective study of the experience of a surgical team with PTC since the Chernobyl accident, taken out of 2349 patients operated on for any thyroid lesions from April 1986 to April 2015, comparing the incidence of PTC by age groups. Main outcome measurement: Comparison of PTC incidence in patients >15 years (group A) and children <15 years (group B) in April 1986. Results: Out of a total of 2349 patients having undergone thyroid surgery for all types of lesions during 30 year after Chernobyl and born before April 1986, 2164 were >15 years of age at the time of the nuclear accident (group A) and 175 developed PTC (8.1%) compared to 36 PTC (19.5%) that occurred in 185 children <15 years of age (group B) in April 1986 (p < 0.001). Conclusions: Radiation exposure affected residents of countries (including Belgium) well beyond Ukraine and Belarus. This was demonstrated by a 1990 meteorological report. Over 30 years, there has been a persistent higher incidence of PTC among Belgian children below the age of 15 years at the time of the Chernobyl accident. This relationship with age has even been strengthened by the implementation of more sophisticated immunohistochemical biomarkers diagnostic technology since April 2011.
    Full-text · Article · Apr 2016
    • "asp). Available data indicates that LDIR can induce cancer (Hatch et al. 2005, Cardis and Hatch 2011, Shah et al. 2012), cataracts (Ainsbury et al. 2009), cardiovascular diseases (Sumner 2007) and long-term psychological consequences (Pastel 2002). With the development of new technologies such as microbeams , irradiation of single cells and investigation of the responses of their neighboring cells with LDIR become possible . "
    [Show abstract] [Hide abstract] ABSTRACT: Purposes: To review research progress on the molecular mechanisms of low dose ionizing radiation (LDIR)-induced hormesis, adaptive responses, radioresistance, bystander effects, and genomic instability in order to provide clues for therapeutic approaches to enhance biopositive effects (defined as radiation-induced beneficial effects to the organism), and control bionegative effects (defined as radiation-induced harmful effects to the organism) and related human diseases. Conclusions: Experimental studies have indicated that Ataxia telangiectasia-mutated (ATM), extracellular signal-related kinase (ERK), mitogen-activated protein kinase (MAPK), phospho-c-Jun NH(2)-terminal kinase (JNK) and protein 53 (P53)-related signal transduction pathways may be involved in LDIR-induced hormesis; MAPK, P53 may be important for adaptive response; ATM, cyclooxygenase-2 (COX-2), ERK, JNK, reactive oxygen species (ROS), P53 for radioresistance; COX-2, ERK, MAPK, ROS, tumor necrosis factor receptor alpha (TNFα) for LDIR-induced bystander effect; whereas ATM, ERK, MAPK, P53, ROS, TNFα-related signal transduction pathways are involved in LDIR-induced genomic instability. These results suggest that different manifestations of LDIR-induced cellular responses may have different signal transduction pathways. On the other hand, LDIR-induced different responses may also share the same signal transduction pathways. For instance, P53 has been involved in LDIR-induced hormesis, adaptive response, radioresistance and genomic instability. Current data therefore suggest that caution should be taken when designing therapeutic approaches using LDIR to induce beneficial effects in humans.
    Full-text · Article · Jun 2014
    • "For example, the release of noxious chemicals may contaminate water, air and soil, disrupting routine social and economic activities and delaying the immediate re-occupation of the community pending a chemical hazard risk assessment [15]. Additionally, health effects from exposure to these noxious chemicals may manifest as both acute and chronic physical or psychological disorders such as cancers [17,18], congenital anomalies [19], asthma [17], emphysema [17], chronic obstructive pulmonary disease [17], cardiovascular outcomes [17], personality/psychiatric disorders [20], endocrine [17], and immune system dysfunction [17,20]. These effects may be magnified in communities already struggling with underlying economic and healthcare vulnerabilities that impair disaster response and recovery [21,22]. "
    [Show abstract] [Hide abstract] ABSTRACT: Community engagement remains a primary objective of public health practice. While this approach has been adopted with success in response to many community health issues, it is rarely adopted in chemical disaster response. Empirical research suggests that management of chemical disasters focuses on the emergency response with almost no community engagement for long-term recovery. Graniteville, an unincorporated and medically underserved community in South Carolina was the site of one of the largest chlorine exposures by a general US population. Following the immediate response, we sought community participation and partnered with community stakeholders and representatives in order to address community-identified health and environmental concerns. Subsequently, we engaged the community through regular town hall meetings, harnessing community capacity, forming coalitions with existing local assets like churches, schools, health centers, and businesses, and hosting community-wide events like health picnics and screenings. Information obtained from these events through discussions, interviews, and surveys facilitated focused public health service which eventually transitioned to community-driven public health research. Specific outcomes of the community engagement efforts and steps taken to ensure sustainability of these efforts and outcomes will be discussed.
    Full-text · Article · Jun 2014
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