Safety to humans

As with all chemicals, including pesticides such as paraquat, care must be taken to minimize human exposure. FAO guidelines for personal protection when working with pesticides in tropical climates can be read here.

Safety instructions on the product label must be read and appropriate personal protective equipment (PPE) used. Normal recommendations are: long-sleeved shirt, long trousers and boots for spraying. The addition of a face shield and gloves are recommended when mixing and handling the concentrated product. Any spills of undiluted product should be washed off the skin immediately and body, clothes and equipment thoroughly washed as normal after spraying.

Provided this care is applied and the product is used as directed, there is no risk to human safety with the use of paraquat. This is the conclusion reached on the basis of extensive laboratory toxicology studies with paraquat and over 50 years of experience in use.

The comments below relate to the acute toxicity of paraquat dichloride (the technical active ingredient). Formulations of paraquat may have different acute toxicity due to dilution of the technical material and the addition of co-formulants.

Paraquat is toxic by the oral route

In their Recommended Classification of Pesticides by Hazard, the World Health Organization (WHO, 2009) classified paraquat as “Moderately hazardous, class II”
In their RED facts document (1997), the US Environmental Protection Agency (EPA) concluded that “paraquat is moderately toxic (Category II) by the oral route”. This category was confirmed in a US EPA risk assessment of 2006. EPA’s website states “Paraquat is highly toxic to humans”.
The European Chemicals Bureau (2004) classified paraquat as “R25, Toxic if swallowed”. According to the current EU regulation 1272/2008, the classification is now Category 3 (H301, "Toxic if swallowed").

Paraquat is slightly toxic by the dermal (skin) route

In a US EPA risk assessment of 2006, US EPA classified paraquat in Category I.
The European Chemicals Bureau (2004) classified paraquat as “R24, Toxic in contact with skin”. According to the current EU regulation 1272/2008, the classification is now Category 3 (H311, "Toxic in contact with skin").

Paraquat is an irritant to skin and eyes

In their evaluation of toxicity for the Joint FAO/WHO Meeting on Pesticide Residues (JMPR, 2003), WHO considered paraquat “to be a mild skin irritant and a moderate eye irritant”.
In a US EPA risk assessment of 2006, US EPA classified paraquat in Category I (eye) and Category III (skin).
The European Chemicals Bureau (2004) classified paraquat as “R36/37/38, irritating to eyes, respiratory system and skin”. According to the current EU regulation 1272/2008, the classification is now Category 2 (H315, "causes skin irritation") for skin irritation, Category 2 (H319, "causes serious eye irritation") for eye irritation and Category 3 for respiratory irritation (STOT SE 3 - H335, "specific organ toxicity single exposure – may cause respiratory irritation").

Paraquat is not a skin sensitizer

In their evaluation of toxicity for the Joint FAO/WHO Meeting on Pesticide Residues (JMPR, 2003), WHO considered paraquat “was not a skin sensitizer in the Magnusson and Kligman test”.
In their RED facts document (1997) the US EPA concluded that paraquat was “not a skin sensitizer under the conditions of the maximization test of B Magnusson and AM Kligman”. This conclusion was confirmed in a US EPA risk assessment of 2006.
In their review report for paraquat, the European Commission (EC, 2003) concluded that paraquat was “negative in Magnusson & Kligman protocol”. According to the criteria used in the current EU regulation 1272/2008, paraquat is not classified as a skin sensitizer.

Paraquat is highly toxic by the inhalation (lungs) route

In their RED facts document, the US EPA (1997) concluded that “paraquat has been shown to be highly toxic by the inhalation route and has been placed in Toxicity Category I (the highest of four levels) for acute inhalation effects. However, the Agency has determined that particles used in agricultural practices (400 to 800μm) are well beyond the respirable range and therefore inhalation toxicity is not a toxicological endpoint of concern.”
The European Chemicals Bureau (2004) classified paraquat as “R26, Very toxic by inhalation”. According to the current EU regulation 1272/2008, the classification is now Category 2 (H330, "Fatal if inhaled").
See below for information about the ability to inhale paraquat into the lungs.

Paraquat is not inhaled into the small airways

Paraquat dichloride is non-volatile and formulations containing paraquat are not applied through spray equipment which generates a significant proportion of respirable spray droplets at the spray nozzle. Paraquat is applied downwards towards the target plant with conventional hydraulic spray equipment for which the droplets produced are generally too large to be inhaled, being typically ~ 200-400μm diameter. Only a small fraction of the total spray droplet distribution leaving the spray nozzle is of respirable size with <0.2% less than 10μm. The inhalable fraction <30μm that is taken into the nose and the mouth during breathing is also too large to reach the alveolar region of the lung. This fraction could, however, be swallowed and is therefore a source of secondary oral ingestion. Mist blowers, which produce large numbers of very fine droplets (50μm and less), are not recommended for spraying paraquat.

In their RED facts document, the US EPA (1997) concluded that for paraquat “particles used in agricultural practices (400 to 800μm) are well beyond the respirable range and therefore inhalation toxicity is not a toxicological endpoint of concern”.

Paraquat is poorly absorbed after oral administration

Specific studies to determine absorption of paraquat after oral administration (Syngenta, unpublished) revealed an absorption factor of 13%. Despite the low absorption rate, oral ingestion of paraquat containing products must be strictly avoided.

In their evaluation of toxicity for the Joint FAO/WHO Meeting on Pesticide Residues (JMPR, 2003), WHO considered paraquat to be “not well-absorbed”
In their RED facts document (1997), the US EPA concluded that “paraquat was poorly absorbed after oral administration to rats, dogs and mice”
In their review report for paraquat, the EC (2003) concluded that paraquat was poorly absorbed with “approximately 10% absorption”

Paraquat cannot readily be absorbed through the skin

Undamaged skin is an effective barrier to paraquat in concentrated or diluted spray-strength solution. Paraquat is water soluble and easily washed off. Prolonged and repeated contact of spray-strength paraquat with skin, through leaking spray equipment or poor personal hygiene can cause skin irritation and even damage in severe cases. These are visible warnings to the user that he or she is doing something wrong and they appear sufficiently early to avoid any further health risk.

In their Reregistration Eligibility Document, RED (1997), the US EPA (1997) concluded that “0.3% of the applied 14C-paraquat dichloride was absorbed through intact skin”
In their review report for paraquat the EC (2003) concluded that the dermal absorption of paraquat was “0.5% based on overall weight of evidence.”

Paraquat is not significantly metabolized

Any absorbed paraquat is generally excreted unchanged with little or no metabolism.

In their evaluation of toxicity for the Joint FAO/WHO Meeting on Pesticide Residues (JMPR, 2003), WHO considered “paraquat is largely eliminated unchanged”.
In their Reregistration Eligibility Decision Document (RED) (1997), the US EPA concluded that “paraquat was not metabolized by rats”.
In their review report for paraquat the EC (2003) concluded that paraquat was subject to “minimal metabolism, representing <1% of recovery”.

Paraquat is rapidly excreted

Paraquat is not stored or accumulated in the body. In occupational circumstances in which very low amounts of the spray-strength product may be absorbed, it is rapidly and effectively eliminated via the urine. In laboratory studies it has been shown that low amounts of absorbed paraquat are rapidly excreted.

In their evaluation of toxicity for the Joint FAO/WHO Meeting on Pesticide Residues (JMPR, 2003), WHO noted that for paraquat “excretion of the radiolabel was rapid; about 90% was excreted within 72h”.
In their Reregistration Eligibility Decision Document (RED) (1997), the US EPA concluded that for paraquat “most of the radioactivity was detected in faeces with 2-3 days after dosing and in urine, within 1 day after dosing”.
In their review report for paraquat, the EC (2003) concluded that the rate of excretion of paraquat was “>90% in 72h”.

Paraquat is not genotoxic in vivo

Paraquat has been evaluated for genotoxic potential in a range of in vitro and in vivo test systems. These studies provide a substantial body of data to indicate that paraquat does not have significant genotoxic potential. Paraquat has produced positive responses in some in vitro assays. These are considered not to be due to paraquat itself, but to the action of paraquat within cellular systems. Paraquat is not genotoxic in higher tier in vivo assays.

In their evaluation of toxicity for the Joint FAO/WHO Meeting on Pesticide Residues (JMPR, 2003), WHO concluded that “paraquat is unlikely to pose a genotoxic risk to humans”.
In their RED facts document, the US EPA (1997) concluded that “paraquat shows no evidence of causing mutagenicity”.
In their review report for paraquat the EC (2003) concluded that genotoxicity studies with paraquat were “negative in vivo. Some in vitro positives”.
In their summary report for paraquat, the Australian Agricultural and Veterinary Chemical Assessment Team Office of Chemical Safety, APVMA (2016) concluded that “The weight-of-evidence indicates that paraquat is non-mutagenic and therefore is not considered to pose a significant genotoxic risk to humans.”

Paraquat is not carcinogenic

The chronic toxicity and potential carcinogenicity of paraquat have been examined in two-year studies in rats and mice. Effects on the lung were the principal effects noted in the chronic feeding studies, which is consistent with the findings from sub-chronic toxicity studies.

In their evaluation of toxicity for the Joint FAO/WHO Meeting on Pesticide Residues (JMPR, 2003), WHO concluded that “the weight of evidence suggested that paraquat was not carcinogenic in the rat. Paraquat was not considered to be tumorigenic in two studies in mice”.
In their Reregistration Eligibility Decision Document (RED) (1997), the US EPA “classified paraquat as a Group E carcinogen (evidence of non-carcinogenicity for humans), based on a lack of evidence of carcinogenicity in acceptable studies with two animal species”.
In their review report for paraquat the EC (2003) concluded that paraquat was “not carcinogenic”.
In their summary report for paraquat, the Australian Agricultural and Veterinary Chemical Assessment Team Office of Chemical Safety, APVMA (2016) concluded that “Long-term feeding studies conducted in mice and rats revealed no evidence that paraquat was carcinogenic.”

Paraquat is not a developmental toxin

No teratogenic potential has been demonstrated in developmental toxicity studies in rats and mice.

In their evaluation of toxicity for the Joint FAO/WHO Meeting on Pesticide Residues (JMPR, 2003), WHO concluded that “teratogenicity was not seen at any dose in any study in either rats or mice”.
In their RED facts document, the US EPA (1997) noted that “the no-observed effect dose levels (NOEL) for maternal toxicity are at least or more conservative (protective) than the NOEL based on developmental toxicity”.
In their review report for paraquat, the EC (2003) concluded that paraquat was only “embryotoxic at maternally toxic doses”.
In their summary report for paraquat, the Australian Agricultural and Veterinary Chemical Assessment Team Office of Chemical Safety, APVMA (2016) concluded that “There was no evidence that paraquat had any teratogenic potential based on a range of studies conducted in mice, rats and rabbits.”

Paraquat is not a reproductive toxin

Paraquat has been demonstrated not to interfere with reproduction in a three-generation reproduction study.

In their evaluation of toxicity for the Joint FAO/WHO Meeting on Pesticide Residues (JMPR, 2003), WHO concluded that “impaired fertility was not seen in these studies”.
In their RED facts document, the US EPA (1997) noted that “there is no evidence that paraquat is associated with reproductive effects”.
In their review report for paraquat, the EC (2003) concluded that reproductive toxicity studies with paraquat demonstrated “no specific effects on reproduction”.
In their summary report for paraquat, the Australian Agricultural and Veterinary Chemical Assessment Team Office of Chemical Safety, APVMA (2016) concluded that “There was no evidence that paraquat caused reproductive toxicity in rats following dietary administration.”

Paraquat is not an endocrine disruptor

The available data for paraquat have been reviewed and are considered not to show evidence of endocrine disruption in: a) Mammalian studies: including rat reproduction (multi-generation); rat and mouse developmental (teratology); one-year dog, lifetime rat and mouse; b) Environmental species: including a life-cycle study in Daphnia and reproduction studies in the bobwhite quail and mallard.

In its report, “Towards the establishment of a priority list of substances for further evaluation of their role in endocrine disruption” for the European Commission DG ENV, BKH Consulting Engineers lists paraquat as a group III substance, which means there is no scientific basis for inclusion on the endocrine disruptor list.

Paraquat is not a neurotoxicity hazard

The neurotoxic potential of paraquat has been extensively studied in laboratory animals. No clinical signs of neurotoxicity or consistent neuropathological changes have been reported following long-term dietary administration of paraquat to rodents or dogs in regulatory-compliant studies.

In their report of a periodic re-evaluation of toxicity for the JMPR (2003) (paraquat), WHO concluded that “studies on the effects of paraquat on the central nervous system have used a variety of routes, including subcutaneous or intraperitoneal injection and direct injection into the central nervous system, and end points observed have been behavioral, morphological and neurochemical. Behavioral effects and loss of neurons in the substantia nigra were observed and, neurochemically, depletion of dopamine was reported in many, but not all, of these studies. However, the design of these studies renders the relevance of these data questionable for the risk assessment of dietary exposure to paraquat residues.” It was then concluded that “the available mechanistic and other animal studies did not support the hypothesis that paraquat residues in food are a risk factor for Parkinson’s disease in humans”
In 2006 US EPA stated “Paraquat does not inhibit cholinesterase activity, produce cholinergic-like toxic signs, or affect morphology of the central or peripheral nervous systems. Furthermore, the molecular structure is not similar to those of compound classes known to have effects on the nervous system. Clinical signs of toxicity did not indicate neurotoxicity. As there is limited concern for neurotoxicity resulting from exposure to paraquat, neurotoxicity studies, including a developmental neurotoxicity study, are not required at this time.”
Paraquat did not result in neurotoxic effects in modern US EPA guideline-compliant oral acute and sub-chronic (90 day) neurotoxicity studies reported in 2006.
In their summary report for paraquat, the Australian Agricultural and Veterinary Chemical Assessment Team Office of Chemical Safety, APVMA (2016) concluded that “The standard toxicological database contains a range of unpublished acute, short-term repeat-dose, subchronic and chronic laboratory studies which do not report any evidence of neurotoxicity in rodents, rabbits or dogs, including any clinical signs (consistent with a proposed neurotoxicant) or neuropathy under the standard suite of pathology tests.”
In the last decade animal studies have focussed on the entry of paraquat into the brain of mice and the potential to cause neuronal cell death in the area of the brain known as the substantia nigra. The main reason for this is the putative link between pesticides and Parkinson’s disease. Please refer to the section below: Paraquat does not cause Parkinson's disease.

Source:

US Environmental Protection Agency, Office of Prevention, Pesticides and toxic substances. 2006. Memorandum: Risk Assessment. Subject: Paraquat Dichloride: Human Health Risk Assessment for Proposed Uses on Ginger and Okra and Amended Uses on Soybeans, Wheat, Cotton, Cucurbits, Onions, and Tanier. PC Code: 061601, Petition Nos: 2F6433, 3E6764, 1E6223, 1E6332, 3E6763, and 1E6319, DP Barcode: D328653.

Paraquat does not cause Parkinson’s disease

The safety of Syngenta’s products for people and the environment is our primary concern. 
We have invested hundreds of millions of dollars over the product lifetime of paraquat to ensure its safety.   
Paraquat has been the subject of more than 1,200 safety studies, submitted to, and reviewed by, regulatory authorities around the world. 
Scientific evidence does not support a link between paraquat and Parkinson’s disease. Syngenta rejects claims made in litigation to the contrary.  
This view is supported by recent thorough reviews performed by the science-based regulatory authorities in Australia and the United States (US).

Background

It is generally agreed among medical experts that a substantial majority of Parkinson’s disease cases have no established cause. In some cases, there are genetic factors associated with the development of Parkinson’s disease. It has also been proposed that a combination of both environmental and genetic factors may contribute to the development of Parkinson’s disease. 

Syngenta position  

Syngenta rejects the claims of a link between paraquat and Parkinson’s disease made in pending litigation because it is not supported by scientific evidence; this is endorsed in science-based reviews by regulatory authorities. Two major authorities have thoroughly reviewed the experimental and human evidence. Both the Australian Pesticides and Veterinary Medicines Authority (APVMA), (2016) and the US Environmental Protection Agency (EPA), (2019) concluded that the evidence does not support a causal relationship between farmers’ use of paraquat and Parkinson’s disease.¹  

The largest, longest-term epidemiological study of agricultural workers and Parkinson’s disease in the US, the Agricultural Health Study (AHS), found no association between exposure to paraquat and Parkinson’s disease (Shrestha, 2020).²

Syngenta has also investigated its own production workers in the UK who were known to have been exposed to paraquat at a manufacturing site and found no increased risk of Parkinson’s disease (Tomenson & Campbell, 2011³ and 2021).⁴  

Similarly, humans exposed to high doses of paraquat, for example through deliberate or accidental ingestion, did not display any Parkinson’s-like symptoms during follow-up.⁵  

Review of reviews  

To examine the extent to which a consensus exists in the scientific community regarding the relationship between exposure to paraquat and Parkinson’s disease, an independent critical review of reviews was undertaken focusing on publications between 2006 and the present (Weed, 2021).⁶ The conclusion was that no such consensus exists in the scientific community and that the available evidence does not warrant a claim that paraquat causes Parkinson’s disease. 

¹ APVMA conclusions were published on the APVMA website on October 26, 2016 https://apvma.gov.au/node/12666 
US Environmental Protection Agency (US EPA) Office of Chemical Safety and Pollution Prevention. Draft Human health Risk Assessment in Support of Registration Review, 26th June 2019 

² Shrestha S, Parks CG, Umbach DM, Richards-Barber M, Hofmann JN, Chen H, Blair A, Beane Freeman LE, Sandler DP. Pesticide use and incident Parkinson's disease in a cohort of farmers and their spouses. Environ Res. 2020 Dec;191:110186. doi: 10.1016/j.envres.2020.110186  https://pubmed.ncbi.nlm.nih.gov/32919961/ 

³ Tomenson, J.A., Campbell, C., 2011. Mortality from Parkinson’s disease and other causes among a workforce manufacturing paraquat: a retrospective cohort study. BMJ Open 1 (2), e00283 http://bmjopen.bmj.com/content/1/2/e000283.full 

⁴ Tomenson, J.A., Campbell, C., 2021. Mortality from Parkinson’s disease and other causes among a workforce manufacturing paraquat: an updated retrospective cohort study. J. Occup. Med. Toxicol. 16, 20 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8157632/ 

⁵ Brent J., Schaeffer T.H. (2011). Systematic Review of Parkinsonian Syndromes in Short- and Long-Term Survivors of Paraquat Poisoning. Journal of Occupational and Environmental Medicine. 53 (11): 1332-1336 http://www.ncbi.nlm.nih.gov/pubmed/21988794 

⁶ Weed DL. Does paraquat cause Parkinson's disease? A review of reviews. Neurotoxicology. 2021 86:180-184. https://doi.org/10.1016/j.neuro.2021.08.006   https://www.sciencedirect.com/science/article/pii/S0161813X21000917?via%... 

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