Cancer - HH-RA.org

Bibliography Tag: cancer

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

Loomis et al., 2015

Dana Loomis, Kathryn Guyton, Yann Grosse, Fatiha El Ghissassi, Véronique Bouvard, Lamia Benbrahim-Tallaa, Neela Guha, Heidi Mattock, Kurt Straif, “Carcinogenicity of lindane, DDT, and 2,4-dichlorophenoxyacetic acid,” The Lancet, 2015, 16, DOI: 10.1016/S1470-2045(15)00081-9.

SUMMARY:

Summarizes the findings of 26 experts from 13 countries who met at the International Agency for Research on Cancer (IARC; Lyon, France) to assess the carcinogenicity of the insecticides lindane and 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane (DDT), and the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) for IARC Monographs Volume 113. 2,4-D was classified as “possibly carcinogenic to humans” (Group 2B) after some studies showed links to cancers including non-Hodgkin’s lymphoma. FULL TEXT

Mostafalou and Abdollahi, 2017

Sara Mostafalou and Mohammad Abdollahi, “Pesticides: an update of human exposure and toxicity,” Archives of Toxicology, February 2017, 91:2, DOI: 10.1007/s00204-016-1849-x.

ABSTRACT:

Pesticides are a family of compounds which have brought many benefits to mankind in the agricultural, industrial, and health areas, but their toxicities in both humans and animals have always been a concern. Regardless of acute poisonings which are common for some classes of pesticides like organophosphoruses, the association of chronic and sub-lethal exposure to pesticides with a prevalence of some persistent diseases is going to be a phenomenon to which global attention has been attracted. In this review, incidence of various malignant, neurodegenerative, respiratory, reproductive, developmental, and metabolic diseases in relation to different routes of human exposure to pesticides such as occupational, environmental, residential, parental, maternal, and paternal has been systematically criticized in different categories of pesticide toxicities like carcinogenicity, neurotoxicity, pulmonotoxicity, reproductive toxicity, developmental toxicity, and metabolic toxicity. A huge body of evidence exists on the possible role of pesticide exposures in the elevated incidence of human diseases such as cancers, Alzheimer, Parkinson, amyotrophic lateral sclerosis, asthma, bronchitis, infertility, birth defects, attention deficit hyperactivity disorder, autism, diabetes, and obesity. Most of the disorders are induced by insecticides and herbicides most notably organophosphorus, organochlorines, phenoxyacetic acids, and triazine compounds.

EPA, 1994a

Environmental Protection Agency, March 2, 1994, Scientific Data Review on Glyphosate and AMPA residues, Office of Prevention, Pesticides, and Toxic Substances.

SUMMARY:

This document contains information to be presented to the Health Effects Division Metabolism Committee at a meeting on March 9, 1994 about Glyphosate and AMPA regulation. FULL TEXT

EPA, 1992b

Environmental Protection Agency, December 15, 1992, “Dietary Exposure Analysis for Glyphosate in Support of the Reregistration Eligibility Document,” Office of Pesticides and Toxic Substances.

SUMMARY:

Memo provides a Dietary Risk Evaluation System for glyphosate as part of the reregistration process. This document confirms that EPA has changed the RfD to 2.0 mg/kg/day. FULL TEXT

EPA, 1991

Environmental Protection Agency, October 30, 1991, Memo on the second peer review of glyphosate oncogenicity, Office of Pesticides and Toxic Substances.

SUMMARY:

This memo reports on the conclusions of the Health Effects Division Carcinogenicity Peer Review Committee meeting of June 26, 1991 where the committee concluded that glyphosate should be classified as Group E- evidence of non-carcinogenicity. Note that three of the committee members did not concur with the decision. FULL TEXT

EPA, 1982a

Environmental Protection Agency, February 9, 1982, Memo on Lifetime Feeding Study in Rats with Glyphosate, Office of Pesticide and Toxic Substances.

ABSTRACT:

Not Available

FULL TEXT

EPA, 1986a

Environmental Protection Agency, March 11, 1986, Memo on Additional Histopathological Evaluations of Chronic Feeding Study of Glyphosate in Mice, Office of Pesticides and Toxic Substances.

SUMMARY:

Report of review of additional pathological and statistical information on mice kidney tumors.

FULL TEXT