Are Herbicides Safe?
Herbicides, also commonly known as weedkillers, are substances used to control unwanted plants. Selective herbicides control specific weed species, while leaving the desired crop relatively unharmed, while non-selective herbicides can be used to clear waste ground, industrial and construction sites, railways and railway embankments as they kill all plant material with which they come into contact. Apart from selective/non-selective, other important distinctions include persistence (also known as residual action: how long the product stays in place and remains active), means of uptake (whether it is absorbed by above-ground foliage only, through the roots, or by other means), and mechanism of action (how it works). Historically, products such as common salt and other metal salts were used as herbicides, however these have gradually fallen out of favor and in some countries a number of these are banned due to their persistence in soil, and toxicity and groundwater contamination concerns. Herbicides have also been used in warfare and conflict.
Modern herbicides are often synthetic mimics of natural plant hormones which interfere with growth of the target plants. The term organic herbicide has come to mean herbicides intended for organic farming. Some plants also produce their own natural herbicides, such as the genus Juglans (walnuts), or the tree of heaven; such action of natural herbicides, and other related chemical interactions, is called allelopathy. Due to herbicide resistance – a major concern in agriculture – a number of products combine herbicides with different means of action. Integrated pest management may use herbicides alongside other pest control methods.
Health and Herbicide
cute toxicity arising from ingestion of a significant quantity rapidly, and chronic toxicity arising from environmental and occupational exposure over long periods. Much public suspicion of herbicides revolves around a confusion between valid statements of acute toxicity as opposed to equally valid statements of lack of chronic toxicity at the recommended levels of usage. For instance, while glyphosate formulations with tallowamine adjuvants are acutely toxic, their use was found to be uncorrelated with any health issues like cancer in a massive US Department of Health study on 90,000 members of farmer families for over a period of 23 years. That is, the study shows lack of chronic toxicity, but cannot question the herbicide’s acute toxicity.
Some herbicides cause a range of health effects ranging from skin rashes to death. The pathway of attack can arise from intentional or unintentional direct consumption, improper application resulting in the herbicide coming into direct contact with people or wildlife, inhalation of aerial sprays, or food consumption prior to the labelled preharvest interval. Under some conditions, certain herbicides can be transported via leaching or surface runoff to contaminate groundwater or distant surface water sources. Generally, the conditions that promote herbicide transport include intense storm events and soils with limited capacity to adsorb or retain the herbicides. Herbicide properties that increase likelihood of transport include persistence (resistance to degradation) and high water solubility.
The risk of Parkinson’s disease has been shown to increase with occupational exposure to herbicides and pesticides. The herbicide paraquat is suspected to be one such factor.
All commercially sold, organic and non-organic herbicides must be extensively tested prior to approval for sale and labeling by the Environmental Protection Agency. However, because of the large number of herbicides in use, concern regarding health effects is significant. In addition to health effects caused by herbicides themselves, commercial herbicide mixtures often contain other chemicals, including inactive ingredients, which have negative impacts on human health.
Reference
Gorell, JM; Johnson, CC; Rybicki, BA; Peterson, EL; Richardson, RJ (1998). “The risk of Parkinson’s disease with exposure to pesticides, farming, well water, and rural living”. Neurology. 50 (5): 1346–50. doi:10.1212/WNL.50.5.1346. PMID 9595985. S2CID 27954760.
Dinis-Oliveira, R.J.; Remião, F.; Carmo, H.; Duarte, J.A.; Navarro, A. Sánchez; Bastos, M.L.; Carvalho, F. (2006). “Paraquat exposure as an etiological factor of Parkinson’s disease”. NeuroToxicology. 27 (6): 1110–22. doi:10.1016/j.neuro.2006.05.012. PMID 16815551.