Pesticide exposure and lymphohaematopoietic cancers: a case-control study in an agricultural region (Larissa, Thessaly, Greece)

Kokouva, Maria; Bitsolas, Nikolaos; Hadjigeorgiou, Georgios M.; Rachiotis, George; Papadoulis, Nikolaos; Hadjichristodoulou, Christos

doi:10.1186/1471-2458-11-5

Cited by 35 publications

(14 citation statements)

References 26 publications

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“…Pesticide exposure exacerbates neurodegeneration in genetically predisposed subjects through mechanisms that involve mitochondrial impairment, redox function and promotion of α‐synuclein aggregation . An association between pesticide exposure and incidence of certain types of cancers, in particular hematopoietic, lung, and prostate cancers has been described . There are concerns about the genotoxic risk associated with long‐term exposure to pesticides as these compounds may damage DNA, resulting in mutations that eventually may lead to cancer, neurological, and reproductive adverse health effects.…”

Section: Introductionmentioning

confidence: 99%

Mechanism underlying the effect of long‐term exposure to low dose of pesticides on DNA integrity

Alleva

Manzella

Gaetani

et al. 2018

Environmental Toxicology

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Pesticides, including herbicides, insecticides and fungicides, are widely used in intensive agriculture. Recently, the long-term effects of pesticide exposure were found to be associated with many diseases. In this study, we evaluated the long-term effect of low-level exposure to a mixture of pesticides on DNA damage response (DDR) in relation to individual detoxifying variability. A residential population chronically exposed to pesticides was enrolled, biological/environmental pesticide levels; paroxonase 1 (PON-1) activity and 192 Q/R polymorphism and DDR were evaluated at three different periods of pesticide exposure. OGG1-dependent DNA repair activity was decreased in relation to pesticide exposure. The increase of DNA lesions and pesticide levels in the intensive pesticide-spraying period was independent on PON-1 activity. Next, human bronchial epithelial and neuronal cells were used as a model for in vitro evaluation of the mechanistic effect of pesticides. Pesticides induced mitochondrial dysfunction leading to ROS formation. ROS from mitochondria induced DNA damage, which in turn induced OGG1-dependent DNA repair activity through 8-oxoguanine DNA glycosylase 1 (OGG1) expression and activation. Even though OGG1 was overexpressed, an inhibition of its activity, associated with DNA lesion accumulation, was found at prolonged pesticide-exposure. A post-translational regulation of OGG1 by pesticide may be postulated. Taken together, long-term exposure to low-levels of pesticides affects DDR resulting in accumulation of DNA lesions that eventually may lead to cancer or neurological disorders.

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Section: Introductionmentioning

confidence: 99%

Mechanism underlying the effect of long‐term exposure to low dose of pesticides on DNA integrity

Alleva

Manzella

Gaetani

et al. 2018

Environmental Toxicology

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“…As a result, 80 articles were potentially eligible; of them 47 provided effect estimates, whereas 33 did not. Letters were sent to the corresponding authors of all 33 articles whose data were insufficient to calculate effect estimates; 16 authors denied the provision of data or declared that they had no available data, nine authors did not reply, whereas the authors of eight studies31–38 provided us with the requested data; as a result, the aforementioned eight studies31–38 have been included in the meta‐analysis.…”

Section: Resultsmentioning

confidence: 99%

Tobacco smoking and risk of multiple myeloma: A meta‐analysis of 40 observational studies

Ψαλτοπούλου

Sergentanis

Kanellias

et al. 2012

Intl Journal of Cancer

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This meta-analysis aims to quantitatively synthesize all available data on the association between tobacco smoking and multiple myeloma (MM) risk. Eligible studies were identified and pooled effect estimates (odds ratios and relative risks) were calculated regarding ever, current and former smoking. Separate analyses were performed on case-control and cohort studies, as well as on males and females. Meta-regression analysis with percentage of males, mean age, years of smoking, pack-years, cigarettes per day, years since quit and age at onset was performed. Forty articles were deemed eligible; of them 27 used a case-control design (4,625 cases and 21,591 controls) and 13 used a cohort design (2,228 incident cases among a total cohort size equal to 1,852,763 subjects). Ever smoking was not associated with MM risk (pooled effect estimate 5 0.92, 95% confidence interval (CI): 0.85-1.00); similar results were obtained for current (pooled effect estimate 5 0.87, 95% CI: 0.74-1.03) and former smoking (pooled effect estimate 5 1.04, 95% CI: 0.96-1.13). Regarding ever smoking, the null association was reproducible upon cohort studies (pooled effect estimate 5 1.01, 95%CI: 0.89-1.15), whereas the inverse association in case-control studies (pooled effect estimate 5 0.87, 95% CI: 0.78-0.96) was particularly due to the bias-prone hospital-based ones. Meta-regression analysis did not yield statistically significant results. In conclusion, MM does not seem to be associated with tobacco smoking. There is a need to further explore how molecular mechanisms are involved in the resistance of MM progenitor cells toward smoking.Multiple myeloma (MM) (plasma cell myeloma, myelomatosis and Kahler's disease) is a mature B-cell neoplastic proliferation, 1 characterized by bone marrow plasmacytosis and overproduction of monoclonal immunoglobulin. This disease is associated with anemia, hypercalcemia, skeletal pain and lytic bone lesions, renal insufficiency, among other related organ or tissue impairment. 2 MM constitutes 10-20% of all hematologic malignancies; its prevalence is expected to rise in Western countries due to the population aging, with 30% of the patients aged more than 75 years. 3 It is estimated that in the US, during 2012, 12,190 men and 9,510 women will be diagnosed and 10,710 men and women will die of myeloma, with a 5-year relative survival of 41%. 4 MM cause remains unclear; there is convincing literature for risk factors, such as increased age, positive family history, male gender and black race, 5 while monoclonal gammopathy of undetermined significance (MGUS) consistently precedes MM. 6 Familial clustering of the disease also suggests a genetic background. 5 Multiple etiologies have been suggested, such as exposure to benzene, petroleum products and to ionizing radiation, as well as agricultural or industrial occupation; on the other hand, conventional cancer causes such as tobacco smoking, obesity and dietary characteristics are probably less implicated. 7,8 Tobacco smoking is among the leading preventable causes...

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“…Pesticide exposure was assessed using a structured pretested questionnaire. 18 Participants provided information regarding all previous neurological conditions, medical problems, illnesses, and current medications. We also collected information regarding the medical history of participants' first-degree relatives, with particular attention to neurological diseases.…”

Section: Study Population and Designmentioning

confidence: 99%

Mediterranean diet adherence is related to reduced probability of prodromal Parkinson's disease

et al. 2018

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Background The International Parkinson and Movement Disorder Society recently introduced a methodology for probability score calculation for prodromal PD. Objectives To assess the probability of prodromal PD in an older population and investigate its possible association with Mediterranean diet adherence. Methods Data from a population‐based cohort study of older adults (HEllenic Longitudinal Investigation of Aging and Diet) in Greece were used. Probability of prodromal PD was calculated according to International Parkinson and Movement Disorder Society research criteria. A detailed food frequency questionnaire was used to evaluate dietary intake and calculate Mediterranean diet adherence score, ranging from 0 to 55, with higher scores indicating higher adherence. Results Median probability of prodromal PD was 1.9%, ranging from 0.2 to 96.7% in 1,731 PD‐free individuals aged ≥ 65 (41% male). Lower probability for prodromal PD (P < 0.001) in the higher Mediterranean diet adherence groups was noted, driven mostly by nonmotor markers of prodromal PD, depression, constipation, urinary dysfunction, and daytime somnolence. Each unit increase in Mediterranean diet score was associated with a 2% decreased probability for prodromal PD (P < 0.001). Compared to participants in the lowest quartile of Mediterranean diet adherence, those in the highest quartile were associated with a ∼21% lower probability for prodromal PD. Conclusions Adherence to the Mediterranean diet is associated with lower probability of prodromal PD in older people. Further studies are needed to elucidate the potential causality of this association, potential relation of the Mediterranean diet to delayed onset or lower incidence of PD, as well as the underlying neurobiological mechanisms. © 2018 International Parkinson and Movement Disorder Society

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Pesticide exposure and lymphohaematopoietic cancers: a case-control study in an agricultural region (Larissa, Thessaly, Greece)

Cited by 35 publications

References 26 publications

Mechanism underlying the effect of long‐term exposure to low dose of pesticides on DNA integrity

Mechanism underlying the effect of long‐term exposure to low dose of pesticides on DNA integrity

Tobacco smoking and risk of multiple myeloma: A meta‐analysis of 40 observational studies

Mediterranean diet adherence is related to reduced probability of prodromal Parkinson's disease

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