Seizures from Chronic Salicylate Intoxication Following Household Exposure to Incense Fumes

Introduction

Salicylates are ubiquitous compounds present in a wide range of over-the-counter and prescription medications, making salicylate toxicity an important cause of morbidity and mortality in children [1]. Aspirin-containing and salicylate-based products – such as topical analgesics (eg, BENGAY®), keratolytic agents containing salicylic acid, oil of wintergreen, and various herbal or medicinal oils – are commonly found in most households, posing a potential risk for accidental exposure or ingestion [2].

The use of aspirin (acetylsalicylic acid) in children has markedly declined following its association with Reye syndrome. Consequently, the incidence of unintentional salicylate intoxication in young children has decreased, aided by regulatory measures such as limiting the aspirin content in chewable, flavored tablets to 81 mg, restricting the number of tablets per bottle to 36, and implementing child-resistant packaging [3–5]. Despite these successes, nontraditional and less-regulated sources of salicylate exposure remain an underrecognized cause of pediatric toxicity.

Incense products have gained popularity in the United States for aromatherapy, cultural practices, and meditation, and are often perceived as harmless. Reports of incense-related salicylate toxicity in children are exceedingly rare, with only isolated cases describing toxicity from non-ingestible household products [6–8]. Similar to prior reports of inadvertent exposure such as salicylate intoxication from teething gel in infancy described by Williams et al [9], this case highlights how commonly used household products may serve as unrecognized sources of chronic toxicity.

The objectives of this report are to describe a rare presentation of pediatric seizures associated with chronic inhalational salicylate exposure from incense, to emphasize the limitations of relying solely on serum salicylate concentrations in chronic toxicity, and to raise awareness of potential regulatory and labeling gaps in salicylate-containing household products.

Case Report

A 3-year-old girl presented to the emergency department following her first episode of a non-febrile, generalized tonic-clonic seizure. The patient had been in her usual state of health until the afternoon of presentation, when her mother observed sudden onset generalized seizure with bilateral upper extremity shaking accompanied by a fixed forward gaze while the child was walking toward the kitchen. The episode lasted approximately 5 minutes. There was no foaming at the mouth, urinary or fecal incontinence, or head trauma.

During transport to our hospital, the patient vomited once in the ambulance. Developmental milestones were appropriate for age; she was able to speak in full sentences in her native language and recognized numbers and body parts. Immunizations were up to date. The parents denied any history of preceding illness, head injury, or known exposure to known toxins.

Emergency Room (ER) assessment was as follows: Patient was in the post-ictal state. Vitals were stable (temperature: 97°F; heart rate: 108 beats/min; respiratory rate: 22 breaths/min; oxygen saturation: 97% on room air). Her weight was 15 kg (75th percentile) and height was 97 cm (75th percentile). She was initially drowsy but became alert and active when her mouth was being examined. The general exam was normal. Muscle tone was normal. Reflexes were 2+ in all 4 limbs. Babinski was a down-going response bilaterally. There was no truncal ataxia or limb dysmetria. Meningeal signs were negative.

ER interventions were as follows: Intravenous line was placed. Serum chemistry revealed metabolic acidosis with preserved renal function and transient stress hyperglycemia; electrolytes including serum magnesium and phosphate levels were otherwise within normal limits (Table 1). Blood work results including blood counts and hepatic profile were within normal limits. She was transferred to the pediatric intensive care unit (PICU) for further evaluation and management.

She had 2 more episodes of seizures while in the PICU. The first episode happened about 2–3 hours after presentation, and was characterized by flexion of both extremities, slight duskiness of the face, and oxygen saturation dropping to 54%. It lasted for about 40 seconds and resolved spontaneously. The second episode happened at 4–5 hours after presentation and was characterized by jerky movements of both extremities associated with frothing from the mouth and oxygen saturation dropping to 39%. It lasted about 7 minutes and aborted after administering lorazepam. Given the recurrence and severity of the seizures, the neurology service recommended continued observation and electroencephalography (EEG), and the patient was loaded with fosphenytoin and initiated on levetiracetam for ongoing seizure control. Between seizure episodes, the patient returned to baseline mental status and maintained normal respiratory rate and oxygenation.

Toxicologic evaluation revealed an elevated initial serum salicylate concentration of 19 mg/dL, which decreased to 17 mg/dL on repeat testing 5 hours later. Urine toxicology screening was negative for other substances. Arterial blood gas analysis demonstrated a mixed respiratory alkalosis with metabolic acidosis (Table 2), with a calculated anion gap of 14 mmol/L. This acid-base pattern is consistent with salicylate toxicity, in which stimulation of the respiratory center leads to hyperventilation and a concurrent metabolic acidosis.

Management was primarily supportive, including close monitoring in the PICU, seizure control with antiseizure medications, and targeted correction of acid-base and electrolyte abnormalities. Initial management included intravenous dextrose 5% in 0.45% sodium chloride with sodium bicarbonate to correct metabolic acidosis and promote urinary alkalinization, thereby enhancing salicylate elimination. Given the risk of potassium depletion associated with salicylate toxicity due to increased renal losses, bicarbonate-containing fluids were replaced with potassium acetate, which serves as a bicarbonate precursor and allows maintenance of alkalinization without excessive sodium bicarbonate administration. Follow-up blood gas measurements during treatment demonstrated normalization, supporting clinical improvement. Serial monitoring revealed a gradual decline in salicylate concentration to 5 mg/dL by the following morning. The observed decline reflects both elimination of the inciting exposure and the effects of targeted treatment. Key interventions occurred after admission and following seizure onset, with subsequent clinical and biochemical improvement. However, precise hourly correlations were not consistently documented.

Neuroimaging with MRI of the brain (with and without contrast) was unremarkable, and EEG was within normal limits. Given the absence of an identifiable acute ingestion and concern for possible chronic environmental exposure, the Poison Control Center and Administration for Children’s Services were notified. A home assessment revealed that incense sticks were being burned regularly in the child’s bedroom over a prolonged period prior to presentation; however, the exact duration of exposure could not be reliably quantified. Information obtained during the home assessment suggested that the identified incense brand may contain salicylates at concentrations of approximately 10–20%, as indicated by product labeling; however, independent laboratory confirmation was not available.

Following cessation of incense use and parental counseling, the patient experienced no further seizures. She was discharged on hospital day 4, with markedly improved salicylate levels. Subsequent follow-up demonstrated complete clinical recovery and normal growth and development.

Discussion

Incense is commonly used in household settings in the United States. Incense formulations may include numerous fragrance ingredients or mixtures thereof. Among these, methyl salicylate has been reported in some incense products at concentrations of approximately 10–20%, and this is of particular toxicologic concern. Other components may include myrrh, cedarwood, cedrol, birch, fir balsam, sandalwood, juniper, benzoin, thyme, eugenol, camphor, cinnamon derivatives, rosemary, clove, and borneol [10,11].

Unlike accidental acute ingestion, incense exposure represents a form of chronic, low-level salicylate exposure through repeated inhalation, particularly in enclosed or poorly ventilated spaces. This distinction is clinically important, as chronic exposure alters both symptom presentation and interpretation of serum salicylate levels. Therapeutic serum salicylate concentrations are generally reported in the range of approximately 10–30 mg/dL when aspirin is intentionally used; however, chronic salicylate toxicity may occur despite serum levels within or below this range, particularly with ongoing exposure. This is because, in chronic salicylate exposure, serum salicylate concentrations do not reliably reflect total body burden or central nervous system penetration [12]. Serum levels may be only mildly elevated or within the therapeutic range despite significant clinical toxicity, due to progressive tissue accumulation over time. In contrast, serum levels in acute ingestion more often correlate with symptom severity. As a result, interpretation of salicylate concentrations, particularly in chronic exposure, must be guided primarily by clinical findings and exposure history rather than absolute serum values [13]. Chronic salicylate intoxication is associated with higher mortality compared with single, acute ingestions [14,15].

Neurologic manifestations, including seizures, are more commonly observed in chronic salicylate toxicity than in acute overdose, and may occur at comparatively lower serum concentrations [16,17]. Central nervous system involvement results from progressive tissue accumulation and increased penetration of non-ionized salicylate across the blood–brain barrier, particularly in the setting of metabolic acidosis [16,18]. Clinical features may include tinnitus, nausea, vomiting, hyperpnea, lethargy, confusion, seizures, cerebral edema, hyperthermia, coma, and death.

In the present case, the absence of a clear ingestion history, the presence of mixed respiratory alkalosis and metabolic acidosis, recurrent seizures, and gradual decline in salicylate levels following cessation of exposure collectively support chronic inhalational toxicity as the most plausible mechanism. Although the differential diagnosis of occult salicylate exposure may include diabetic ketoacidosis, sepsis, pneumonia, iron intoxication, ethylene glycol ingestion, and ethanol intoxication, identification of an elevated serum salicylate concentration obviated the need for further diagnostic evaluation for these conditions.

Following ingestion or inhalation, salicylates are rapidly absorbed through the gastrointestinal and respiratory mucosa. Acetylsalicylic acid is rapidly hydrolyzed to salicylic acid, its active metabolite. Salicylic acid is efficiently absorbed in the stomach and small intestine, metabolized primarily in the liver, and eliminated within approximately 2–3 hours at therapeutic doses. Salicylate toxicity can involve multiple organ systems, including the central nervous, cardiovascular, pulmonary, hepatic, renal, and metabolic systems. Its pathogenic effects arise largely from interference with cellular energy metabolism: salicylates uncouple oxidative phosphorylation, inhibit enzymes of the Krebs cycle, and disrupt amino acid synthesis. These biochemical derangements lead to increased oxygen consumption, heat production, metabolic acidosis, and a wide spectrum of clinical manifestations [7,19,20].

Although most clinical data on salicylate toxicity derive from oral or systemic exposure, regulatory toxicology assessments provide important insights into the biological plausibility of inhalational toxicity from volatile salicylates such as methyl salicylate. While direct human inhalation absorption data are lacking, inhalational absorption is expected based on the physicochemical properties of methyl salicylate, with subsequent systemic distribution and hydrolysis to salicylic acid [21]. Repeated inhalation exposure to methyl salicylate has been evaluated primarily in animal studies. These studies demonstrate that inhalation is a biologically relevant route of exposure, with dose-dependent systemic and neurologic effects observed in some repeated-dose animal models, although findings are limited by older study designs and methodological constraints. While direct human data and quantitative pharmacokinetic measurements following inhalation are lacking, these regulatory data support the plausibility of systemic effects following repeated inhalational exposure, particularly with prolonged or unrecognized contact. Taken together, these mechanistic and regulatory findings provide a framework for interpreting the present case, in which chronic, occult inhalational exposure was suspected in the absence of intentional ingestion [22].

Beyond its clinical implications, this case highlights important regulatory and public health gaps related to salicylate-containing household products, particularly those intended for non-ingestible use such as incense. Unlike over-the-counter medications, which are subject to standardized labeling, dosing restrictions, and child-resistant packaging, many household and consumer fragrance products are regulated inconsistently or classified in ways that do not require clear disclosure of potentially toxic constituents. As a result, caregivers may be unaware that commonly used products can serve as sources of clinically significant salicylate exposure, especially with repeated use in enclosed environments. Additionally, greater awareness among clinicians is essential, as chronic environmental exposure may not be identified through routine history-taking unless specifically queried. Incorporating questions about household products, aromatics, and incense use into evaluations of unexplained metabolic acidosis or neurologic symptoms may facilitate earlier diagnosis and reduce morbidity.

Conclusions

Chronic salicylate intoxication in children can present subtly yet carry life-threatening consequences. All salicylate-containing products should include clear and standardized warning labels. Currently, many incense products and candles marketed for household use in the United States lack appropriate labeling regarding their salicylate content and potential toxicity. A detailed environmental history including prolonged incense use in enclosed spaces should be considered in any child presenting with unexplained seizures with concurrent acid-base imbalance. It is essential that nurses, physicians, pharmacists, and families remain aware of this potential risk to prevent avoidable toxic exposures.