Mode of Carcinogenic Action of Pesticides Inducing Thyroid Follicular Cell Tumors in Rodents

Hurley, Pamela M.; Hill, Richard N.; Whiting, Rick J.

doi:10.2307/3434175

Cited by 45 publications

(58 citation statements)

References 11 publications

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“…In terms of etiology, the causative agent for the observed increase in thyroid cancer mortality is uncertain. To date, no pesticides have been proven to be carcinogenic to the human thyroid (25,27). Heavy use of chlorophenoxy herbicides in western Minnesota creates concern for elevated dioxin levels in this population.…”

Section: Discussionmentioning

confidence: 99%

“…Mechanistically, ETU decreases thyroxine and increases thyroidstimulating hormones, as well as causes thyroid and liver neoplasms in rodents. ETU is a thyroid peroxidase inhibitor in rodent studies, disrupting the thyroid-pituitary homeostasis (25,27). Besides their effect on the thyroid, EBDCs are also teratogenic in rodents, causing damaging effects in the gonads of both male and female rats, which successful for the more common forms of this disease, with a 5-year survival rate of over 90% (23)(24)(25).…”

Section: Discussionmentioning

confidence: 99%

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Cancer Mortality in Agricultural Regions of Minnesota

Schreinemachers

Creason²,

Garry³

1998

Epidemiology

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cancer Mortality in Agricultural Regions of Minnesota

Schreinemachers

Creason²,

Garry³

1998

Epidemiology

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“…The 2,6-dinitroaniline herbicides (which include benfluralin, trifluralin, ethalfluralin, oryzalin pendimethalin, and prodiamine) were associated with elevated risk of mild hypospadias. These compounds are moderately volatile, with vapor pressures higher than 10 5 mm Hg at 25°C (ie, high potential for exposure via volatilization drift), they are lipophilic, their use was frequent (11% of controls were exposed), and trifluralin, [37][38][39] prodiamine, 40 and pendimethalin 40,41 are suspected endocrine disruptors. Chloracetanilide herbicides (metolachlor, acetochlor, and alachlor) and polyalkyloxy compounds used as adjuvants were associated with elevated risk of moderate to severe hypospadias.…”

Section: Discussionmentioning

confidence: 99%

Hypospadias and Residential Proximity to Pesticide Applications

2013

PEDIATRICS

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WHAT'S KNOWN ON THIS SUBJECT: Some studies suggest a contribution of environmental exposures such as pesticides to risk of hypospadias, whereas others do not. One of the challenges that has limited current knowledge is the lack of detailed exposure data. WHAT THIS STUDY ADDS:This study examined a more detailed assessment of exposure to pesticides than previous studies. Exposure assignments, whether to groups of chemicals, specific chemicals, or a composite involving a number of chemicals, showed a general lack of association with hypospadias. abstract BACKGROUND: Experimental evidence suggests pesticides may be associated with hypospadias.OBJECTIVE: Examine the association of hypospadias with residential proximity to commercial agricultural pesticide applications. METHODS:The study population included male infants born from 1991 to 2004 to mothers residing in 8 California counties. Cases (n = 690) were ascertained by the California Birth Defects Monitoring Program; controls were selected randomly from the birth population (n = 2195). We determined early pregnancy exposure to pesticide applications within a 500-m radius of mother' s residential address, using detailed data on applications and land use. Associations with exposures to physicochemical groups of pesticides and specific chemicals were assessed using logistic regression adjusted for maternal race or ethnicity and age and infant birth year.RESULTS: Forty-one percent of cases and controls were classified as exposed to 57 chemical groups and 292 chemicals. Despite .500 statistical comparisons, there were few elevated odds ratios with confidence intervals that excluded 1 for chemical groups or specific chemicals. Those that did were for monochlorophenoxy acid or ester herbicides; the insecticides aldicarb, dimethoate, phorate, and petroleum oils; and adjuvant polyoxyethylene sorbitol among all cases; 2,6-dinitroaniline herbicides, the herbicide oxyfluorfen, and the fungicide copper sulfate among mild cases; and chloroacetanilide herbicides, polyalkyloxy compounds used as adjuvants, the insecticides aldicarb and acephate, and the adjuvant nonyl-phenoxy-poly(ethylene oxy)ethanol among moderate and severe cases. Odds ratios ranged from 1.9 to 2.9.CONCLUSIONS: Most pesticides were not associated with elevated hypospadias risk. For the few that were associated, results should be interpreted with caution until replicated in other study populations.

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“…Previous reproductive toxicity tests in rats using a number of conazoles reported testicular atrophy, prostate atrophy, reproductive failure and cancers of the thyroid and pituitary gland and liver. Conazoles have demonstrated CYP450 modulation, which led to the idea that their toxicity may be nuclear receptor-mediated (Hurley, 1998;Nelson et al, 2004).…”

Section: Car and Pxr In Drug Induced Liver Injurymentioning

confidence: 99%

Genomic Profiling in Nuclear Receptor-Mediated Toxicity

2007

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Nuclear receptors (NRs) are attractive drug targets due to their role in regulation of a wide range of physiologic responses. In addition to providing therapeutic value, many pharmaceutical agents along with environmental chemicals are ligands for NRs and can cause adverse health effects that are directly related to activation of NRs. Identifying the molecular events that produce a toxic response may be confounded by the fact that there is a significant overlap in the biological processes that NRs regulate. Microarrays and other methods for gene expression profiling have served as useful, sensitive tools for discerning the mechanisms by which therapeutics and environmental chemicals invoke toxic effects. The capability to probe thousands of genes simultaneously has made genomics a prime technology for identifying drug targets, biomarkers of exposure/toxicity and key players in the mechanisms of disease. The complex intertwining networks regulated by NRs are hard to probe comprehensively without global approaches and genomics has become a key technology that facilitates our understanding of NR-dependent and -independent events. The future of drug discovery, design and optimization, and risk assessment of chemical toxicants that activate NRs will inevitably involve genomic profiling. This review will focus on genomics studies related to PPAR, CAR, PXR, RXR, LXR, FXR, and AHR.

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Mode of Carcinogenic Action of Pesticides Inducing Thyroid Follicular Cell Tumors in Rodents

Cited by 45 publications

References 11 publications

Cancer Mortality in Agricultural Regions of Minnesota

Cancer Mortality in Agricultural Regions of Minnesota

Hypospadias and Residential Proximity to Pesticide Applications

Genomic Profiling in Nuclear Receptor-Mediated Toxicity

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