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Abstract

Introduction

The toxicity and carcinogenicity of glyphosate have long been debated. Nevertheless, the mortality rate in patients with acute glyphosate-surfactant poisoning varies across different groups.

Methods

Between 2002 and 2020, 109 patients with glyphosate-surfactant poisoning received treatment at Chang Gung Memorial Hospital. Patients were stratified into two subgroups according to their prognosis: good (n = 74) or poor (n = 35). Baseline demographics, psychiatric comorbidities, medical complications, and laboratory data were collected, and mortality data were analyzed.

Results

The patients were 54.1 ± 17.5 years of age and were mostly male (68.8%). Most patients (91.7%) ingested pesticides intentionally, and patients arrived at the hospital within 7.1 ± 12.7 h. Psychiatric comorbidities were prevalent, and the top three comorbidities were mental (71.6%), depressive (48.6%), and adjustment (14.7%) disorder. Patients with poor prognoses were older than those with good prognoses (p = .007). Moreover, patients with poor prognoses had lower Glasgow Coma Scale scores (p < .001) and diastolic blood pressure (p = .008), but higher incidences of upper gastrointestinal bleeding (p < .001), aspiration pneumonia (p < .001), hypotension (p < .001), hyperglycemia (p = .002), acute kidney injury (p < .001), and metabolic acidosis (p < .001) than patients with good prognoses. The mortality rate was 5.5%. A multivariate-logistic-regression model revealed that the Glasgow Coma Scale score was a significant risk factor for poor prognosis (odds ratio 0.653, confidence interval 0.427–0.998; p = .049). However, no risk factors for mortality were identified.

Conclusions

A total of 32.1% of patients with glyphosate-surfactant poisoning had poor prognoses, and 5.5% of patients died despite treatment. The mortality outcome is comparable to that of published reports from other international poison centers.

Keywords

Glyphosate-surfactant pesticide poisoning suicide psychiatric comorbidity mortality

Introduction

Glyphosate surfactants are nonselective herbicides used extensively for controlling broadleaf weeds and grasses worldwide. It is believed that glyphosate has minimal toxicity because the target enzyme 5-enolpyruvylshikimate 3-phosphate synthase is present in plants and microorganisms, but not in humans.¹ Moreover, the lethal dose of glyphosate in experimental rats is more than 4320 mg per kg body weight when ingested orally and is thought to have low toxicity.²

The toxicity and carcinogenicity of glyphosate surfactants have long been debated.³ The International Agency for Research on Cancer announced that glyphosate is a Group 2A carcinogen in 2015.⁴ Importantly, the International Agency for Research on Cancer reported strong data indicating that both pure glyphosate and glyphosate surfactants can cause genetic damage. In contrast, the U.S. Environmental Protection Agency argued that there is no evidence linking glyphosate to cancer in humans and that glyphosate use does not pose any health risks.⁵ The European Union also stated that under conditions of approval and by following good agricultural practices, glyphosate is considered not to have any harmful effects on human health or unacceptable effects on the environment.⁶ Furthermore, Ye et al.⁷ suggested that caution is needed in the regulation of glyphosate pesticides because the replacement herbicides could cause more harm to humans.

Suicide by pesticide poisoning is a common way of committing suicide and is a vital public health problem in Asia. A review of the literature (Table 1) revealed that the intentional ingestion of glyphosate commonly occurs in Asia, which could be due to the ease of pesticide access. In the case of acute high-dose exposure to glyphosate-surfactant herbicides, the mortality rates varied widely from 1.8% to 46.0%.^8–25 The lowest mortality rate was reported by Seok et al.,¹⁷ and the highest mortality rate was reported by Zouaoui et al.¹⁸ This discrepancy could be due to patient and treatment heterogeneity. Nonetheless, the large variation in mortality across different hospitals has triggered our interest and prompted us to analyze our poisoning registry database.

Table 1.

Literature data on the mortality outcomes of patients with glyphosate-surfactant poisoning.

Year	Study	Area	Sample size	Age (year)	Mortality rate (%)
1988	Sawada et al⁸	Japan	56	47	16.1
1991	Tominack et al⁹	Taiwan	97	35 ± 15	11.3
1991	Talbot et al¹⁰	Taiwan	93	37 ± 17	7.5
1997	Hung et al¹¹	Taiwan	53	41 ± 17	1.9
2000	Lee et al¹²	Taiwan	131	48 ± 2	8.4
2008	Lee et al¹³	Taiwan	58	48.8 ± 15.8	29.3
2009	Chen et al¹⁴	Taiwan	2186	42.8 ± 18.6	7.2
2010	Roberts et al¹⁵	Sri Lanka	601		3.2
2010	Moon et al¹⁶	Korea	76	55.1 ± 16.3	2.6
2011	Seok et al¹⁷	Korea	107	52.3 ± 15.5	1.8
2013	Zouaoui et al¹⁸	France	13	58.7 ± 8.8	46
2013	Chen et al¹⁹	Taiwan	24	56.8 ± 17.6	8.3
2014	Kim et al²⁰	Korea	153	56	12.4
2015	Kamijo et al²¹	Japan	117		6.8
2016	Kim et al²²	Korea	232		12.5
2016	Mohamed et al²³	Sri Lanka	270		3.3
2019	Cho et al²⁴	Korea	150	59.9 ± 14.5	9.3
2022	Ahn et al²⁵	Korea	424		10.1
2024	Present study	Taiwan	109	54.1 ± 17.5	5.5

This observational study investigated the mortality data of Taiwanese patients with glyphosate-surfactant poisoning and compared these data with published studies of glyphosate-surfactant poisoning from other poison centers.

Materials and methods

Patients

Between 2002 and 2020, a total of 109 patients with glyphosate-surfactant poisoning received treatment at Chang Gung Memorial Hospital. The following data for each patient were collected: age, sex, exposure route, time between ingestion and hospital arrival, systemic diseases such as hypertension, diabetes mellitus, stroke, coronary artery disease, chronic obstructive pulmonary disease, chronic kidney disease or malignancy, smoking habits, alcohol consumption, psychiatric comorbidities, clinical manifestations, vital signs, hemograms, biochemistry, arterial blood gas, length of hospital stay, length of intensive care unit stay, respiratory failure, cardiac arrest, and mortality. The designation of exposure routes was based on the patients’ clinical history. Pesticide containers were obtained from family members for confirmation of glyphosate-surfactant ingestion. Baseline demographics, psychiatric comorbidities, medical complications, and laboratory data were collected, and mortality data were analyzed.

Patient groups

Patients were categorized into two subgroups based on their clinical prognosis: good (n = 74) or poor (n = 35). Patients who had a favorable outcome without severe complications were defined as having a good prognosis, whereas those who died or experienced significant complications such as intensive care unit admission, cardiac arrest, acute kidney injury, or respiratory failure were grouped as having a poor prognosis.

Inclusion and exclusion criteria

All patients with glyphosate-surfactant poisoning treated at our Poison Center were included. Patients were excluded from this research if they co-ingested other pesticides or if the exposure route was not oral.

Clinical diagnosis

The diagnosis of glyphosate-surfactant poisoning was based on the pesticide exposure history, clinical manifestations, physical examination results, and laboratory findings. As blood and urine glyphosate tests were not available, a meticulous clinical history was obtained, which included inquiring the patient and families about the herbicide information and requesting the container for verification.

Clinical management

Patients were treated with gastric lavage using 2 L of normal saline, followed by activated charcoal administration given by a nasogastric tube. Gastric lavage was indicated if the patient arrived at the hospital 1 hour after pesticide intake. The contraindications for gastric lavage involve deficits in airway protective responses, swallowing of a corrosive acid/alkali substance, or the hazard of alimentary tract hemorrhage due to a primary disease. The purpose of activated charcoal administration was to prevent further gastrointestinal absorption. Since there is a lack of antidotes for patients with glyphosate-surfactant poisoning, clinical management is largely supportive of symptoms.

Statistical analysis

Comparisons between the good and poor prognosis groups were performed via t test for quantitative variables and chi-square tests for categorical variables. Univariate binary logistic regression analysis was carried out to examine the clinical and laboratory variables that might be linked with poor prognosis or mortality. To avoid the influence of confounders, a multivariate regression analysis was carried out to investigate the significant variables during the univariate analysis. A p value of less than 0.05 was considered statistically significant. The analysis was performed with IBM SPSS Statistics for Windows, version 25.0. (Armonk, New York, United States, 2017).

Results

The average age of the patients was 54.1 ± 17.5 years (Table 2), and most patients were male (68.8%). Most of the patients intentionally ingested glyphosate surfactants (91.7%), and patients arrived at the hospital in 7.1 ± 12.7 h. Hypertension and diabetes mellitus were noted in 29.4% and 15.6% of patients, respectively. Patients with poor prognoses were older than the patients with good prognoses (60.6 ± 17.8 vs 51.0 ± 16.6 years, p = .007). Apart from this, no other differences were noted between the two groups.

Table 2.

Baseline characteristics of patients with glyphosate-surfactant poisoning stratified into two subgroups according to their prognosis: good or poor (n = 109).

Variable	All patients (n = 109)	Good prognosis group (n = 74)	Poor prognosis group (n = 35)	p Value
Age, year	54.1 ± 17.5	51.0 ± 16.6	60.6 ± 17.8	0.007**
Male, n (%)	75 (68.8)	48 (64.9)	27 (77.1)	0.269
Intentional ingestion, n (%)	100 (91.7)	68 (91.9)	32 (91.4)	1.000
Time between ingestion and hospital arrival, hour	7.1 ± 12.7	8.8 ± 15.1	3.8 ± 3.2	0.083
Hypertension, n (%)	32 (29.4)	18 (24.3)	14 (40.0)	0.116
Diabetes mellitus, n (%)	17 (15.6)	9 (12.2)	8 (22.9)	0.166
Old stroke, n (%)	11 (10.1)	9 (12.2)	2 (5.7)	0.497
Coronary artery disease, n (%)	4 (3.7)	2 (2.7)	2 (5.7)	0.592
Chronic obstructive pulmonary disease, n (%)	1 (0.9)	0 (0)	1 (2.9)	0.324
Chronic kidney disease, n (%)	12 (11)	5 (6.8)	7 (20.0)	0.052
Malignancy, n (%)	7 (6.4)	6 (8.1)	1 (2.9)	0.426
Smocking habit, n (%)	31 (28.4)	21 (28.4)	10 (28.6)	1.000
Alcohol consumption, n (%)	46 (42.2)	31 (41.9)	15 (42.9)	1.000

Note: **p < .01.

Psychiatric comorbidities were prevalent in pesticide-treated patients after consultation-liaison psychiatric evaluation (Table 3). The top three psychiatric comorbidities were mental disorders (71.6%), depressive disorders (48.6%), and adjustment disorders (14.7%). There were higher percentages of psychotic disorders (11.4% vs 1.4%, p = .036) and delirium or dementia (11.4% vs 1.4%, p = .036) in patients with poor prognoses than in patients with good prognoses.

Table 3.

Psychiatric comorbidities of patients with glyphosate-surfactant poisoning stratified into two subgroups according to their prognosis: good or poor (n = 109).

Variable	All patients (n = 109)	Good prognosis group (n = 74)	Poor prognosis group (n = 35)	p Value
Mental disorder, n (%)	78 (71.6)	55 (74.3)	23 (65.7)	0.371
Adjustment disorder, n (%)	16 (14.7)	12 (16.2)	4 (11.4)	0.577
Depressive disorder, n (%)	53 (48.6)	39 (52.7)	14 (40.0)	0.227
Bipolar disorder, n (%)	3 (2.8)	3 (4.1)	0 (0)	0.550
Psychotic disorder, n (%)	5 (4.6)	1 (1.4)	4 (11.4)	0.036*
Substance disorder, n (%)	2 (1.8)	1 (1.4)	1 (2.9)	0.541
Alcohol use disorder, n (%)	10 (9.2)	7 (9.5)	3 (8.6)	1.000
Delirium or dementia, n (%)	5 (4.6)	1 (1.4)	4 (11.4)	0.036*
Deferred, n (%)	2 (1.8)	0 (0)	2 (5.7)	0.101

Note: *p < .05.

After pesticide ingestion (Table 4), the patients developed many medical complications, such as consciousness disturbance (Glasgow Coma Scale score 13.6 ± 3.2), nausea or vomiting (41.3%), hyperglycemia (35.8%), aspiration pneumonia (34.9%), metabolic acidosis (28.4%), tachycardia (28.4%), acute kidney injury (25.7%), colic (21.1%), hypotension (13.8%), noncardiogenic pulmonary edema (11.0%), upper gastrointestinal bleeding (10.1%), etc. Moreover, patients with poor prognoses had lower Glasgow coma scale scores (p < .001) and diastolic blood pressures (p = .008), but higher incidences of upper gastrointestinal bleeding (p < .001), aspiration pneumonia (p < .001), hypotension (p < .001), hyperglycemia (p = .002), acute kidney injury (p < .001), and metabolic acidosis (p < .001) than patients with good prognoses. No differences in other clinical variables were noted between the two groups.

Table 4.

Clinical findings of patients with glyphosate-surfactant poisoning stratified into two subgroups according to their prognosis: good or poor (n = 109).

Variable	All patients (n = 109)	Good prognosis group (n = 74)	Poor prognosis group (n = 35)	p Value
Vital signs
Heart rate, bpm	92.3 ± 17.9	91.7 ± 18.4	93.5 ± 16.9	0.632
Systolic blood pressure, mmHg	132.6 ± 30.7	135.3 ± 29.2	126.8 ± 33.3	0.184
Diastolic blood pressure, mmHg	81.1 ± 18.6	84.4 ± 15.6	74.3 ± 22.5	0.008**
Body temperature, °C	36.2 ± 2.1	36.3 ± 2.4	36.0 ± 1.10	0.630
Neurological system
Glasgow Coma scale, score	13.6 ± 3.2	14.8 ± 1.3	11.2 ± 4.4	<0.001***
Gastrointestinal system
Nausea or vomiting, n (%)	45 (41.3)	33 (44.6)	12 (34.3)	0.405
Colic, n (%)	23 (21.1)	17 (23.0)	6 (17.1)	0.618
Diarrhea, n (%)	12 (11.0)	5 (6.8)	7 (20.0)	0.052
Upper gastrointestinal bleeding, n (%)	11 (10.1)	1 (1.4)	10 (28.6)	<0.001***
Acute pancreatitis, n (%)	1 (0.9)	0 (0.0)	1 (2.9)	0.321
Respiratory system
Aspiration pneumonia, n (%)	38 (34.9)	16 (21.6)	22 (62.9)	<0.001***
Noncardiogenic pulmonary edema, n (%)	12 (11.0)	5 (6.8)	7 (20.0)	0.052
Cardiovascular system
Tachycardia, n (%)	31 (28.4)	20 (27.0)	11 (31.4)	0.655
Bradycardia, n (%)	3 (2.8)	2 (2.7)	1 (2.9)	1.000
Hypotension, n (%)	15 (13.8)	3 (4.1)	12 (34.3)	<0.001***
Endocrine system
Hyperglycemia (glucose >120 mg/dL)	39 (35.8)	19 (25.7)	20 (57.1)	0.002**
Genitourinary system
Acute kidney injury, n (%)	28 (25.7)	0 (0)	28 (80)	<0.001***
Metabolic acidosis, n (%)	31 (28.4)	8 (10.8)	23 (65.7)	<0.001***

Note: bpm beat per minute, **p < .01, ***p < .001.

Laboratory data (Table 5) revealed that patients with a poor prognosis had greater white blood cell counts (p = .009), urea nitrogen (p = .018), creatinine (p = .018), glucose (p = .004), arterial pH (p < .001), and bicarbonate (p < .001) levels than patients with a good prognosis did.

Table 5.

Laboratory findings of patients with glyphosate-surfactant poisoning stratified into two subgroups according to their prognosis: good or poor (n = 109).

Variable	All patients (n = 109)	Good prognosis group (n = 74)	Poor prognosis group (n = 35)	p Value
Hemoglobin, g/dL	14.1 ± 2.5	14.1 ± 2.3	14.1 ± 2.9	0.975
Hematocrit, %	41.4 ± 6.9	41.2 ± 6.3	41.7 ± 7.8	0.730
White blood cell count, 1000/uL	12.3 ± 4.8	11.2 ± 4.5	13.9 ± 4.9	0.009**
Platelets, 1000/uL	248.2 ± 83.9	256.2 ± 96.4	236.5 ± 60.8	0.289
Blood urea nitrogen, mg/dL	19.3 ± 19.7	14.2 ± 10.5	26.7 ± 26.7	0.018*
Creatinine, mg/dL	1.3 ± 1.5	1.0 ± 0.59	1.7 ± 2.2	0.018*
Sodium, mEq/L	139.0 ± 14.1	140.4 ± 3.9	137.0 ± 22.0	0.260
Alanine aminotransferase, U/L	30.7 ± 23.2	27.9 ± 19.7	37.7 ± 27.8	0.068
Random glucose, mg/dL	155.1 ± 70.9	135.5 ± 64.8	187.0 ± 70.0	0.004**
Arterial blood gas
PH	7.4 ± 0.1	7.4 ± 0.1	7.3 ± 0.1	<0.001***
Partial pressures of carbon dioxide, mmHg	36.7 ± 9.4	37.9 ± 9.2	35.0 ± 9.6	0.205
Bicarbonate, mm/L	20.3 ± 4.6	22.6 ± 3.1	16.9 ± 4.4	<0.001***

Note: *p < .05, **p < .01, ***p < .001.

The mortality rate was 5.5% (Table 6). Acute respiratory failure and cardiac arrest developed in 16.5% and 7.3% of patients, respectively. In addition, patients with poor prognoses had longer hospitalization periods than patients with good prognoses did (p < .001).

Table 6.

Outcomes of patients with glyphosate-surfactant poisoning intoxication stratified into two subgroups according to their prognosis: good or poor (n = 109).

Variable	All patients (n = 109)	Good prognosis group (n = 74)	Poor prognosis group (n = 35)	p Value
Respiratory failure, n (%)	18 (16.5)	0 (0)	18 (51.4)	<0.001***
Cardiac arrest, n (%)	8 (7.3)	0 (0)	8 (22.9)	<0.001***
Mortality, n (%)	6 (5.5)	0 (0)	6 (17.1)	0.001**
Length of hospital stay, day	6.6 ± 6.5	4.5 ± 4.5	10.9 ± 7.7	<0.001***
Length of intensive care unit stay, day	1.1 ± 3.5	0 ± 0	3.5 ± 5.5	<0.001***

Note: **p < .01, ***p < .001.

The data were analyzed using a multivariate logistic regression model (Table 7), and the results indicated that the Glasgow Coma Scale score was an important risk factor for poor prognosis (odds ratio 0.653, confidence interval 0.427-0.998, p = .049) in patients with glyphosate-surfactant poisoning. However, no mortality predictors were found.

Table 7.

Prediction of poor prognosis via logistic regression analysis.

Variable	Univariate analysis			Multivariate analysis
Variable	Odds ratio	95% confidence interval	p Value	Odds ratio	95% confidence interval	p Value
Age (per 1-year increase)	1.034	1.008–1.060	0.009**	0.962	0.893–1.037	0.317
Glasgow Coma scale (per 1-score increase)	0.616	0.483–0.787	<0.001***	0.653	0.427–0.998	0.049*
Upper gastrointestinal bleeding (yes)	29.412	3.559–250	0.002**	0.998	0.000 -	0.998
Aspiration pneumonia (yes)	6.135	2.545–14.706	<0.001***	1.106	0.130–9.419	0.927
Hypotension (yes)	12.346	3.205–47.619	<0.001***	1.473	0.029–75.701	0.847
Metabolic acidosis (yes)	15.873	5.747–43.478	<0.001***	6.289	0.721–55.556	0.096
White blood cell count (per 1-1000/uL increase)	1.139	1.026–1.265	0.015*	1.046	0.896–1.221	0.571
Creatinine (per 1-mg/dL increase)	6.346	1.799–22.383	0.004**	2.214	0.657–7.455	0.200
Glucose (per 1-mg/dL increase)	5.263	1.517–18.182	0.009**	1.019	0.996–1.043	0.101

Note: *p < .05, **p < .01, ***p < .001.

Discussion

This study contributes to the literature by demonstrating that acute, large-dose exposure to glyphosate-surfactant herbicides could cause significant mortality and morbidity. Among the 109 patients, 35 (32.1%) had poor prognoses, and the overall mortality rate was 5.5%. As shown in Table 1, the mortality data are comparable to published data from international poison centers, for which the mortality rates ranged between 1.8% and 46.0%.^8–25

The analytical data indicate that lower Glasgow Coma Scale scores in individuals exposed to glyphosate surfactants may be a predictor of a poor prognosis. Other investigators also suggested that glyphosate exposure can lead to a loss of consciousness and lower Glasgow Coma Scale scores^15,22,25 and that the pesticide may also induce seizures.¹⁵ Several types of neurologic damage caused by glyphosate have been reported in previous studies. Animal studies have shown that exposure to glyphosate can result in changes in gene regulation and neurotransmitter levels in the cerebrum, leading to neurotoxicity in the forebrain and midbrain regions of zebrafish.²⁶ An in vitro study revealed that treatment with high concentrations of glyphosate can negatively affect the integrity of the blood–brain barrier, leading to alterations in neuron metabolic processes and glucose uptake by cerebral vascular endothelial cells, resulting in neurological damage.²⁷ Glyphosate also affects serotonin, dopamine, and norepinephrine concentrations in the cerebrum and modifies monoamine neurotransmitters in a regional- and dose-associated way, according to a laboratory study.²⁸ Studies have suggested that glyphosate has a potent toxic effect on cerebral transmission and causes oxidative stress, inflammation, and mitochondrial malfunction. These biological activities can eventually result in neuronal mortality through mechanisms such as autophagy, necrosis, or apoptosis and trigger behavioral symptoms in addition to motor neuron disease.²⁹ These findings may help explain the observed changes in Glasgow Coma Scale scores in this study.

A total of 28 (25.7%) patients experienced acute kidney injury after glyphosate-surfactant poisoning. Renal complications have been reported in other studies ^{19, 25, 30.} In this study, 11 patients were found to have both acute kidney injury and hypotension when they visited the emergency room; therefore, a prerenal form with reduced blood flow to the kidney was considered. However, reports have indicated the direct kidney toxicity of the surfactant used in this herbicide.³⁰ In a laboratory study,³¹ Ma et al. reported that glyphosate exposure modified the transcription of immunoglobulin M, complement C3, and lysozyme in the kidneys of common carp and caused renal damage, such as vacuolization of the kidney parenchyma and intumescence of the kidney tubules. In a clinical study, Mohamed et al. suggested that elevated urinary levels of cytochrome C and interleukin-18 after glyphosate-surfactant self-poisoning could help in the diagnosis of acute kidney injury and confirm glyphosate-surfactant-induced renal apoptosis and mitochondrial toxicity.²³ Kimura et al. published a clinical case of acute kidney injury after glyphosate and surfactant ingestion. A biopsy of the patient’s kidneys revealed damage to the tubular epithelium, specifically in the proximal tubules. Pathology revealed vacuolization of the proximal tubular epithelium, which was noted throughout the biopsied sample.^30,32 Therefore, the mitochondrial damage caused by glyphosate could be associated with acute kidney injury, and the combination of glyphosate and surfactants could damage vascular endothelial cells and produce circulatory insufficiency.

In this study, 38 out of 109 patients (34.9%) experienced aspiration pneumonia, and 12 patients (11.0%) had non-cardiogenic pulmonary edema. Significant laryngeal injury was noted after glyphosate intoxication and was strongly correlated with aspiration pneumonitis and significantly longer hospital stays.¹¹ Another study showed that after the ingestion of glyphosate, various degrees of corrosive esophageal injury from 1 to 2b were noted.¹⁹ This study revealed that 10.1% of patients had upper gastrointestinal bleeding. The pain related to corrosive injury may contribute to swallowing difficulty and choking, and some patients with upper gastrointestinal bleeding also experience coffee ground vomiting, all of which can lead to aspiration pneumonia. Additionally, gastric lavage with activated charcoal in the emergency room may also be a potential contributor.³³ Previous studies have reported that pulmonary edema is an uncommon complication of glyphosate poisoning.³⁴ However, in our study, 12 patients (11.0%) experienced non-cardiogenic pulmonary edema. Overall, 16.5% of patients experienced respiratory failure necessitating ventilatory support. Several studies have shown that glyphosate can induce inflammation in pulmonary and airway tissues, triggering increased levels of eosinophils, neutrophils, and asthma-associated cytokines (interleukin-5, interleukin-10, interleukin-13, interleukin-33, and thymic stromal lymphopoietin), which cause airway tightening.^35,36 One study suggested that lung and kidney toxicity are the main contributing factors to the mortality of patients who are poisoned by glyphosate.¹³ Pulmonary toxicity, in particular, appears to be a critical factor according to the above studies.

The majority of patients intentionally ingested glyphosate-surfactant herbicides (91.7%, Table 2). Psychiatric comorbidities were prevalent (Table 3), and the top three comorbidities were mental disorders (71.6%), depressive disorders (48.6%), and adjustment disorders (14.7%). Studies have shown that glyphosate-surfactant poisoning is always associated with suicide attempts in Asia.^{9,13,17,19,20,22} To date, no studies have explored the correlation between glyphosate poisoning and underlying psychiatric illnesses. This is the first study to analyze the psychiatric comorbidities of glyphosate-surfactant-treated patients to identify the underlying psychiatric patterns. A previous systematic review³⁷ revealed that a high proportion of people who self-harm has a psychiatric disorder, highlighting the need to include appropriate psychological and/or pharmaceutical interventions in their post-incident care.

The limitations of this study include its retrospective nature, small sample size, lack of data on urine/blood glyphosate levels, lack of data on surfactants, and short follow-up duration. However, further studies are needed.

Conclusions

A total of 32.1% of patients with glyphosate-surfactant poisoning had poor prognoses, and 5.5% of these patients died despite intensive treatment. A prompt diagnosis of glyphosate-surfactant poisoning and an immediate institution of a treatment protocol are necessary. Moreover, the mortality outcome is comparable to that of published reports from other international poison centers.

Footnotes

Author contributions

K.H.L. data collection and manuscript writing; S.S.C., C.Y.T., H.Y.C., W.C.L., P.Y.K., K.F.T., J.C.Y. data analysis; I.K.W. manuscript editing; T.H.Y. study supervision, patient care and management. All the authors have read and agreed to the published version of the manuscript.

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was supported by grants from Chang Gung Memorial Hospital (CORPG3N0391 and CORPG3K0195).

Ethical statement

ORCID iDs

Hsien-Yi Chen

Tzung-Hai Yen

Data Availability Statement

The datasets used or analyzed in the study are available from the corresponding author upon reasonable request.

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Human poisoning with glyphosate-surfactant herbicides: Retrospective analysis of mortality outcomes of patients treated in a poison center

Abstract

Introduction

Methods

Results

Conclusions

Keywords

Introduction

Materials and methods

Patients

Patient groups

Inclusion and exclusion criteria

Clinical diagnosis

Clinical management

Statistical analysis

Results

Discussion

Conclusions

Footnotes

Author contributions

Declaration of conflicting interests

Funding

Ethical statement

ORCID iDs

Data Availability Statement

References