Cancer Pesticide residues on food do not cause cancer. Some medical research has suggested
glyphosate exposure may cause cancer, but there is no good evidence of this, even with high-level exposure. Agricultural workers exposed to high levels of synthetic pesiticide have an increased prevalence of some cancers (including
lymphoma and
prostate cancer), and a decreased prevalence of others.
Neurological A review of multiple studies that looked at high pesticide exposure, mainly organophosphates, among agricultural workers suggested an association with various neurological disorders, but the evidence was weak. Comparable studies have not been done with newer pesticides that are replacing organophosphates.
In-utero and early-childhood exposure There is accumulating evidence of neurological effects secondary to pesticide exposure. Acute exposure to high levels of pesticides that affect the central nervous system can cause neurotoxicity, including cognitive and motor changes. in particular because some pesticides and their metabolites cross the placenta and fetal blood-brain-barrier, which has not fully developed in a fetus.
Parkinson's disease and Alzheimer's disease An accumulation of chronic exposure has been associated with an increased risk of developing neurodegenerative disease later in life. There is strong evidence that chronic exposure to pesticides increases risk of developing Parkinson's disease, potentially through direct toxic effects on dopaminergic neurons (which are depleted in Parkinson's disease).
Organochlorines specifically have been linked with autism.
Reproductive effects Many pesticides act as endocrine-disrupting chemicals (EDC) or substances that interfere with normal hormonal activity. As of 2013, 101 pesticides have been listed as proven or possible
endocrine disruptors. As such, high levels of and/or long-term exposure to pesticides can impact reproductive health and is associated with decreased fertility, increased rates of miscarriage, and changes in pattern of maturity. Specifically, triazines, organs-chlorine, and carbamate insecticides have anti-androgenic effects impacting males, resulting in the lack of development of male characteristics including decreases in testicular size, sperm production, and androgen production. Pesticide exposure resulted in reduced fertility in males, genetic alterations in sperm, a reduced number of sperm, damage to germinal epithelium and altered hormone function. The effects of endocrine disruption is dependent on the timing of pesticide exposure (for example, during embryogenesis in early pregnancy or in infancy) as windows of varying susceptibility dictate disease manifestation. Maternal exposure to pesticides has also been linked to higher incidence of hypospadias in the newborn, which is the abnormal opening of the urethra in males. A significant association was found between exposure to pesticides and decreased lung function along with related airway symptoms. Decreased lung function was associated with occupational exposure to pesticides. Studies have suggested a correlation between inhibition of cholinesterase by pesticides like carbamate and organophosphate and reduction or impairment of lung function. In addition, exposure to pesticides was also reported to be linked with obstructive and restrictive lung conditions. Specifically, organophosphate exposure was associated with lung function decline driven by a restrictive process.
Other Some studies have found increased risks of
dermatitis in those exposed. There is increasing evidence that possibly suggests increased risk of development of
type 2 diabetes with exposure to pesticides and their metabolites. ==Prevention==