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Bibliography Tag: cancer

Kriebel et al., 2016

David Kriebel, ScD, Polly J. Hoppin, ScD, Molly M. Jacobs, MPH, Richard W. Clapp, DSc, “Environmental and Economic Strategies for Primary Prevention of Cancer in Early Life,” Pediatrics, 2016, 138:s1, DOI: 10.1542/peds.2015-4268

ABSTRACT:

This article summarizes the evidence for environmental toxic exposures contributing to cancers in early life, focusing on the most common cancer sites in this age group. It provides examples of widespread avoidable exposures to human carcinogens through air, water, and food and then describes recent examples of successful initiatives to reduce exposure to chemicals linked to these cancer sites, through government policy, industry initiatives, and consumer activism. State government initiatives to reduce toxic chemical exposures have made important gains; the Toxics Use Reduction Act of Massachusetts is now 25 years old and has been a major success story. There are a growing number of corporate initiatives to eliminate toxics, especially carcinogens, from the products they manufacture and sell. Another important opportunity for cancer prevention is provided by online databases that list chemicals, their toxicity, and lower-toxicity alternatives; these can be used by businesses, health care institutions, consumers, and workers to reduce exposures to chemicals of concern. The article concludes by inviting pediatricians and public health professionals to include elimination of carcinogen exposures in their work to promote primary prevention of cancer in early life. FULL TEXT

Weichenthal et al., 2010

Scott Weichenthal, Connie Moase, and Peter Chan, “A Review of Pesticide Exposure and Cancer Incidence in the Agricultural Health Study Cohort,” Environmental Health Perspectives, 118, DOI: 10.1289/ehp.0901731

ABSTRACT:

OBJECTIVE: We reviewed epidemiologic evidence related to occupational pesticide exposures and cancer incidence in the Agricultural Health Study (AHS) cohort.

DATA SOURCES: Studies were identified from the AHS publication list available at http://aghealth.nci.nih.gov as well as through a Medline/PubMed database search in March 2009. We also examined citation lists. Findings related to lifetime-days and/or intensity-weighted lifetime-days of pesticide use are the primary focus of this review, because these measures allow for the evaluation of potential exposure–response relationships.

DATA SYNTHESIS: We reviewed 28 studies; most of the 32 pesticides examined were not strongly associated with cancer incidence in pesticide applicators. Increased rate ratios (or odds ratios) and positive exposure–response patterns were reported for 12 pesticides currently registered in Canada and/or the United States (alachlor, aldicarb, carbaryl, chlorpyrifos, diazinon, dicamba, S-ethyl-N,N-dipropylthiocarbamate, imazethapyr, metolachlor, pendimethalin, permethrin, trifluralin). However, estimates of association for specific cancers were often imprecise because of small numbers of exposed cases, and clear monotonic exposure–response patterns were not always apparent. Exposure misclassification is also a concern in the AHS and may limit the analysis of exposure–response patterns. Epidemiologic evidence outside the AHS remains limited with respect to most of the observed associations, but animal toxicity data support the biological plausibility of relationships observed for alachlor, carbaryl, metolachlor, pendimethalin, permethrin, and trifluralin.

CONCLUSIONS: Continued follow-up is needed to clarify associations reported to date. In particular, further evaluation of registered pesticides is warranted.

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Avila-Vazquez et al., 2017

Medardo Avila-Vazquez, Eduardo Maturano, Agustina Etchegoyen, Flavia Silvina Difilippo, Bryan Maclean, “Association between Cancer and Environmental Exposure to Glyphosate,” International Journal of Clinical Medicine, 2017, 8:2, DOI: 10.4236/ijcm.2017.82007

ABSTRACT:

BACKGROUND: Argentina, Brazil, Paraguay and Uruguay farm transgenic seeds glyphosate resistant. Argentina annually utilizes 240,000 tonnes of glyphosate in agriculture. A change in the profile of morbidity and mortality is perceived in agricultural areas; cancer seems to prevail. Monte Maíz is a typical argentine agricultural town with 8000 inhabitants; the Mayor and residents of Monte Maiz requested an environmental health study due to perceived increase in cancer frequencies.

METHODS: An exploratory ecological study was developed to assess the urban environmental contamination and the frequencies and distribution of cancer through an environmental analysis of pollution sources including measurements of pesticides in water, soil and grain dust, and a cross-sectional study of cancer patients that explore associations with different variables.

RESULTS: Glyphosate was detected in soil and grain dust and was found to be at an even higher concentration in the village soil than in the rural area. 650 tonnes are used annually in the region and manipulated inner town. We do not find other relevant sources of pollution. Cancer incidence, prevalence, and mortality are between two and three times higher than the reference values (Globocan 2012, WHO) for the entire nation (706/100,000 persons vs. 217/100,000; 2123/100,000 persons vs. 883.82/100,000 and 383/100,000 persons vs. 115.13/100,000, respectively).

CONCLUSION: This study detects high glyphosate pollution in association with increased frequencies of cancer in a typical argentine agricultural village, and by design, cannot make claims of causality. Other study designs are required, but if we corroborate the concrescence of high exposure to glyphosate and cancer. FULL TEXT

Avila-Vazquez et al., 2015

Medardo Avila-Vazquez, Agustina Etchegoyen, Eduardo Maturano and Luciana Ruderman, “Cancer and detrimental reproductive effects in an Argentine agricultural community environmentally exposed to glyphosate,” The Journal of Biological Physics and Chemistry, 2015, 15:3, DOI: 10.4024/09VA15A.jbpc.15.03

ABSTRACT:

Argentina utilizes about 200 000 tonnes of glyphosate for its agriculture each year. People living near the fields treated with glyphosate often mention an increase in cancer and reproductive alterations. In Monte Maiz, an agricultural settlement with approximate population 8000, we conducted an environmental test assessing water, soil and particulate material contamination as well as an epidemiological study to detect and locate cases of cancer, abortion and genetic abnormality. The site utilizes annually 650 tonnes of glyphosate applied over an area of 65 000 ha. The glyphosate is concentrated and prepared for dispersal in the settlement. We detected glyphosate in particulate material and grain husks and it was found to be present at an even higher concentration on the ground in the village than in the surrounding rural area. The rate of spontaneous abortion in Monte Maiz is three times higher than the national average and the rate of occurrence of genetic abnormality is about twice the national average. Cancer occurrence is between two and three times the reference values for the entire nation with regard to incidence, prevalence and mortality. Although it is of course impossible to establish direct causality, the indicators that emerge from the correlated variables strongly suggest a public health problem of significant proportions, requiring immediate attention.

Di Renzo et al., 2015

Gian Carlo Di Renzo, Jeanne A. Conry, Jennifer Blake, Mark S. DeFrancesco, Nathaniel DeNicola, James N. Martin Jr., Kelly A. McCue, David Richmond, Abid Shah, Patrice Sutton, Tracey J. Woodruff, Sheryl Ziemin van der Poel, Linda C. Giudice, “International Federation of Gynecology and Obstetrics opinion on reproductive health impacts of exposure to toxic environmental chemicals,” International Journal of Gynecology and Obstetrics, 2015, 131, DOI: 10.1016/j.ijgo.2015.09.002

ABSTRACT:

Exposure to toxic environmental chemicals during pregnancy and breastfeeding is ubiquitous and is a threat to healthy human reproduction. There are tens of thousands of chemicals in global commerce, and even small exposures to toxic chemicals during pregnancy can trigger adverse health consequences. Exposure to toxic environmental chemicals and related health outcomes are inequitably distributed within and between countries; universally, the consequences of exposure are disproportionately borne by people with low incomes. Discrimination, other social factors, economic factors, and occupation impact risk of exposure and harm. Documented links between prenatal exposure to environmental chemicals and adverse health outcomes span the life course and include impacts on fertility and pregnancy, neurodevelopment, and cancer. The global health and economic burden related to toxic environmental chemicals is in excess of millions of deaths and billions of dollars every year. On the basis of accumulating robust evidence of exposures and adverse health impacts related to toxic environmental chemicals, the International Federation of Gynecology and Obstetrics (FIGO) joins other leading reproductive health professional societies in calling for timely action to prevent harm. FIGO recommends that reproductive and other health professionals advocate for policies to prevent exposure to toxic environmental chemicals, work to ensure a healthy food system for all, make environmental health part of health care, and champion environmental justice. FULL TEXT

Eriksson et al., 2008

Mikael Eriksson, Lennart Hardell, Michael Carlberg and Måns Åkerman, “Pesticide exposure as risk factor for non-Hodgkin lymphoma including histopathological subgroup analysis,” International Journal of Cancer, 2008, 123, DOI: 10.1002/ijc.23589

ABSTRACT:

We report a population based case–control study of exposure to pesticides as risk factor for non-Hodgkin lymphoma (NHL). Male and female subjects aged 18–74 years living in Sweden were included during December 1, 1999, to April 30, 2002. Controls were selected from the national population registry. Exposure to different agents was assessed by questionnaire. In total 910 (91%) cases and 1016(92%) controls participated. Exposure to herbicides gave odds ratio(OR) 1.72, 95% conﬁdence interval (CI) 1.18–2.51. Regarding phenoxyacetic acids highest risk was calculated for MCPA; OR 2.81,95% CI 1.27–6.22, all these cases had a latency period >10 years.Exposure to glyphosate gave OR 2.02, 95% CI 1.10–3.71 and with>10 years latency period OR 2.26, 95% CI 1.16–4.40. Insecticides overall gave OR 1.28, 95% CI 0.96–1.72 and impregnating agents OR 1.57, 95% CI 1.07–2.30. Results are also presented for different entities of NHL. In conclusion our study conﬁrmed an association between exposure to phenoxyacetic acids and NHL and the association with glyphosate was considerably strengthened. FULL TEXT

De Roos et al., 2003

A J De Roos, S Zahm, K Cantor, D Weisenburger, F Holmes, L Burmeister, and A Blair, “Integrative assessment of multiple pesticides as risk factors for non-Hodgkin’s lymphoma among men,” Occupational and Environmental Medicine, 2003, 60:9, DOI: 10.1136/oem.60.9.e1

ABSTRACT:

METHODS: During the 1980s, the National Cancer Institute conducted three case-control studies of NHL in the midwestern United States. These pooled data were used to examine pesticide exposures in farming as risk factors for NHL in men. The large sample size (n = 3417) allowed analysis of 47 pesticides simultaneously, controlling for potential confounding by other pesticides in the model, and adjusting the estimates based on a prespecified variance to make them more stable.

RESULTS: Reported use of several individual pesticides was associated with increased NHL incidence, including organophosphate insecticides coumaphos, diazinon, and fonofos, insecticides chlordane, dieldrin, and copper acetoarsenite, and herbicides atrazine, glyphosate, and sodium chlorate. A subanalysis of these “potentially carcinogenic” pesticides suggested a positive trend of risk with exposure to increasing numbers.

CONCLUSION: Consideration of multiple exposures is important in accurately estimating specific effects and in evaluating realistic exposure scenarios. FULL TEXT

Band et al., 2011

Band PR, Abanto Z, Bert J, Lang B, Fang R, Gallagher RP, Le ND., “Prostate cancer risk and exposure to pesticides in British Columbia farmers,” Prostate, 2011, 71:2, DOI: 10.1002/pros.21232.

ABSTRACT:

BACKGROUND: Several epidemiologic studies have reported an increased risk of prostate cancer among farmers. Our aim was to assess the risk of developing prostate cancer in relation to exposure to specific active compounds in pesticides.

METHOD: A case-control approach was used with 1,516 prostate cancer patients and 4,994 age-matched internal controls consisting of all other cancer sites excluding lung cancer and cancers of unknown primary site. Lifetime occupational history was obtained through a self-administered questionnaire and used in conjunction with a job exposure matrix to estimate the participants’ lifetime cumulative exposure to approximately 180 active compounds in pesticides. Conditional logistic regression was used to assess prostate cancer risk, adjusting for potential confounding variables and effect modifiers. These include age, ethnicity, alcohol consumption, smoking, education, and proxy respondent.

RESULTS AND CONCLUSIONS: The significant association between prostate cancer risk and exposure to DDT (OR = 1.68; 95% CI: 1.04-2.70 for high exposure), simazine (OR = 1.89; 95% CI: 1.08-3.33 for high exposure), and lindane (OR = 2.02; 95% CI: 1.15-3.55 for high exposure) is in keeping with those previously reported in the literature. We also observed a significant excess risk for several active ingredients that have not been previously reported in the literature such as dichlone, dinoseb amine, malathion, endosulfan, 2,4-D, 2,4-DB, and carbaryl. Some findings in our study were not consistent with those reported in the literature, including captan, dicamba, and diazinon. It is possible that these findings showed a real association and the inconsistencies reflected differences of characteristics between study populations.

Waddell et al., 2001

Waddell BL, Zahm SH, Baris D, Weisenburger DD, Holmes F, Burmeister LF, Cantor KP, Blair A., “Agricultural use of organophosphate pesticides and the risk of non-Hodgkin’s lymphoma among male farmers (United States).,” Cancer Causes Control, 2001, 12:6.

ABSTRACT:

OBJECTIVE: Data from three population-based case-control studies conducted in Kansas, Nebraska, Iowa, and Minnesota were pooled to evaluate the relationship between the use of organophosphate pesticides and non-Hodgkin’s lymphoma (NHL) among white male farmers.

METHODS: The data set included 748 cases of non-Hodgkin’s lymphoma and 2236 population-based controls. Telephone or in-person interviews were utilized to obtain information on the use of pesticides. Odds ratios (OR) adjusted for age, state of residence, and respondent status, as well as other pesticide use where appropriate, were estimated by logistic regression.

RESULTS: Use of organophosphate pesticides was associated with a statistically significant 50% increased risk of NHL, but direct interviews showed a significantly lower risk (OR = 1.2) than proxy interviews (OR = 3.0). Among direct interviews the risk of small lymphocytic lymphoma increased with diazinon use (OR = 2.8), after adjustment for other pesticide exposures.

CONCLUSIONS: Although we found associations between the risk of NHL and several groupings and specific organophosphate pesticides, larger risks from proxy respondents complicate interpretation. Associations, however, between reported use of diazinon and NHL, particularly diffuse and small lymphocytic lymphoma, among subjects providing direct interviews are not easily discounted.

Cabello et al., 2001

Gertrudis Cabello, Mario Valenzuela, Arnaldo Vilaxa, Viviana Durán, Isolde Rudolph, Nicolas Hrepic, and Gloria Calaf, “A Rat Mammary Tumor Model Induced by the Organophosphorous Pesticides Parathion and Malathion, Possibly through Acetylcholinesterase Inhibition,” Environmental Health Perspectives, 2001, 109:5.

ABSTRACT:

Environmental chemicals may be involved in the etiology of breast cancers. Many studies have addressed the association between cancer in humans and agricultural pesticide exposure. Organophosphorous pesticides have been used extensively to control mosquito plagues. Parathion and malathion are organophosphorous pesticides extensively used to control a wide range of sucking and chewing pests of field crops, fruits, and vegetables. They have many structural similarities with naturally occurring compounds, and their primary target of action in insects is the nervous system; they inhibit the release of the enzyme acetylcholinesterase at the synaptic junction. Eserine, parathion, and malathion are cholinesterase inhibitors responsible for the hydrolysis of body choline esters, including acetylcholine at cholinergic synapses. Atropine, a parasympatholytic alkaloid, is used as an antidote to acetylcholinesterase inhibitors. The aim of this study was to examine whether pesticides were able to induce malignant transformation of the rat mammary gland and to determine whether alterations induced by these substances increase the cholinergic activation influencing such transformation. These results showed that eserine, parathion, and malathion increased cell proliferation of terminal end buds of the 44-day-old mammary gland of rats, followed by formation of 8.6, 14.3, and 24.3% of mammary carcinomas, respectively, after about 28 months. At the same time, acetylcholinesterase activity decreased in the serum of these animals from 9.78 +/- 0.78 U/mL in the control animals to 3.05 +/- 0.06 U/mL; 2.57 +/- 0.15 U/mL; and 3.88 +/- 0.44 U/mL in the eserine-, parathion-, and malathion-treated groups, respectively. However, atropine alone induced a significant (p < 0.05) decrease in the acetylcholinesterase activity from the control value of 9.78 +/- 0.78 to 4.38 +/- 0.10 for atropine alone, to 1.32 +/- 0.06 for atropine in combination with eserine, and 2.39 +/- 0.29 for atropine with malathion, and there was no mammary tumor formation. These results indicate that organophosphorous pesticides induce changes in the epithelium of mammary gland influencing the process of carcinogenesis, and such alterations occur at the level of nervous system by increasing the cholinergic stimulation. FULL TEXT

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