Toxicities of Cannabis Volatile Emissions from Cultivation

January 8, 2026

Toxicities of Cannabis Volatile Emissions from Cultivation

Respiratory Irritation

Toxic and Carcinogenic Levels of ß-Myrcene

(Updated from October 18, 2024 Report)

SUMMARY Volatile emissions released from cannabis plants during cultivation are known to cause respiratory harm, including irritation of the lower and upper respiratory track. Up to 70% of workers at indoor facilities without proper protection reported respiratory irritation, half with asthma, which can be serious, even fatal. Residents, customers and workers near outdoor cultivation fields breathe these same volatile cannabis emissions and have also experienced respiratory illness. Workers, often performing strenuous activities, on or near outdoor cultivation fields have increased exposure due to increased respiratory rates. Although workers are exposed 40-60 hr/week, residents are exposed to high emission levels continuously during flowering and harvest, often 6 months/year with two growth cycles.

Furthermore, one of the dominant volatile compounds released during cultivation, the terpene ß-Myrcene, is a potent carcinogen listed on California’s Proposition 65, in addition to its irritant properties. Scientific analyses confirm that people living or working near cannabis fields are exposed to high levels of ß-Myrcene, in the range that caused toxicities and ultimately cancer in laboratory animals. Children are particularly vulnerable, as they are more susceptible to all air pollutants.

Analyzing odors can be achieved with quantitative scientific methods in real time in the field (e.g., gas chromatography), thus avoiding subjective and varying determinations by human nasal receptors. Multiple studies have defined that necessary mitigation is to attenuate odors by long separation distances. Thus, policy makers have the tools necessary to require mitigations to protect public health: either sufficiently long setbacks to prevent terpenes from leaving the cultivation parcel or only allowing indoor/greenhouse cultivation with appropriate filters, both in conjunction with quantitative terpene monitoring.

I. TOXICITIES OF CANNABIS EMISSIONS DURING CULTIVATION

The Neighborhood Coalition1 has confirmed that published literature shows that inhalation of cannabis emissions causes respiratory harm [1-8,41] including asthma which can lead to deaths. Children are at greater risk of respiratory harm as they are more susceptive to air pollutants [45].

People often find odors from cannabis cultivation objectionable. These emissions are not mere annoyances. They have resulted in immediate deleterious effects (including in cannabis workers) encompassing nausea, headaches, cough, eye irritation, respiratory distress and asthma, including two deaths from asthma [2-7, 17, 41]. Up to 70% of cannabis workers reported respiratory irritation with half of those reporting asthma [4]. Neighbors are exposed to these same cannabis emissions but are exposed 24/7 (168 hr/wk), thus 4 times the exposure time as workers who are only exposed 40 hr/wk. In addition, workers on adjacent agricultural lands are exposed for 40-60 hr/wk.

ß-Myrcene is also contained in Hops used in beer manufacture; it was found to be the sensitizing agent in a brewery inspector employee with respiratory hypersensitivity [8].

Real-life experience confirms that exposure to even low levels of cannabis cultivation odor causes physical illness (nausea, respiratory irritation, headache, aggravation of asthma) and prevents residents from using their yards or opening their windows. In addition to the confirmed toxicities of cannabis cultivation emissions, a dominant component in cannabis emissions, ß-Myrcene, inhaled by people living near outdoor cannabis cultivation sites can reach amounts that may be toxic and carcinogenic [3]. The risks are likely even greater for children and fetuses in utero.

ß-Myrcene is listed under Proposition 65 as a cancer-causing compound [9]2 and also showed toxic effects in rodents on liver and kidney after only 3 months [3]. Neighbors living and working near an outdoor cannabis cultivation operation are involuntarily exposed to cannabis emissions that contain this toxin and carcinogen. ß-Myrcene also contributes to formation of secondary toxic pollutants in the air including formaldehyde [10], also a carcinogen listed on Proposition 65, and formic acid, both of which cause eye irritation and nausea [11]. It also leads to formation of ground-level ozone [12, 37], also a known irritant.

Volatile cannabis emissions are greatest during flowering and harvest [13, 37]. Often cannabis harvest occurs at the same time as harvest on adjacent parcels, increasing exposure; inhalation of these emissions by farm workers also increases their health risks. Exposures are amplified when winds are blowing toward workers or residences. Anyone who smells cannabis is being exposed to ß-Myrcene by inhalation, which is a direct and rapid route for small lipophilic compounds to enter the bloodstream [14] as well as to cross the blood-brain barrier entering the brain [50, 51].

The longer the exposure and the higher the concentrations, the greater the toxicity and cancer risk to individuals. The amount of ß-Myrcene inhaled in a single season may cause liver or kidney toxicity and over several years can exceed the carcinogenic dose determined through controlled tests with animals [3]. Children are subject to greater risk due to higher exposure per body weight, increased respiratory rate, and their developing lungs and more rapidly dividing cells as they grow. During pregnancy, terpenes inhaled in cannabis emissions can cross the placenta [15, 53] and the developing fetus may be exposed to significantly greater amounts of ß-Myrcene than the mother on a relative body-weight basis.

Cannabis emission and terpenes have been shown to travel over 3000 ft in the absence of wind [16] and up to 2 miles ([42] including data from Kern County Cannabis EIR and Kram report]). Air dispersion models show very high odor levels from a 1-acre grow [Figure 3-1 in ref 42, including data from Yolo County Cannabis EIR]: at 100 ft, 30 Odor Units (~600-1500 parts per billion (ppb) ß-Myrcene [21]); at 1000 ft, 5 Odor Units (~100-250 ppb ß-Myrcene), and even at 2500 ft, 2.5 Odor Units (~50-125 ppb ß-Myrcene). This projection is for flat topography with no wind or air inversions. Depending on the proximity to the neighboring properties, size of the cultivation field, wind direction, local topography, and prevailing climatic conditions, appropriate separation distances for neighbors, farmworkers and businesses (e.g., winery tasting rooms) from outdoor cannabis fields can require thousands of feet from the cannabis operation. This problem is compounded when multiple grows are in close proximity.

Analyzing odors can be achieved with quantitative scientific methods in real time in the field (e.g., gas chromatography) [21], thus avoiding subjective and often varying determinations by human nasal receptors. Toxic/safe limits can be set using conversion from toxic levels in animal studies to equivalent human dosing levels, using methodology employed by pharmaceutical industry, toxicologists, and FDA (Appendix; [33], [Appendix C in ref 42]).

II. TOXICITY OF ß-MYRCENE

A. Animal Toxicity Testing

Toxicity testing in rodents is a normal first step before testing a new drug candidate in people. The National Toxicology Program (NTP) decided to test ß-Myrcene in animal carcinogenicity models due to its use as a flavoring food additive (albeit in very small amounts) and its structural similarity to D-limonene, another terpene that NTP had previously tested [35].

The NTP studies of ß-Myrcene showed toxicity and clear evidence of carcinogenicity in animal testing: it caused toxicity (kidney and liver) in rodents by oral gavage after 3 months and at 2 years caused liver and kidney cancers in mice and rats, respectively, at the lowest dose tested [3]. Toxicity increased in the animal studies with duration of dosing from 3 weeks to 2 years, including liver and kidney toxicities, chronic inflammation, bone marrow and lymph node atrophy, and tissue necrosis. At the highest dose tested, all animals died within a week. At the 2-year point, liver and kidney cancers were present at the lowest dose.

A subchronic (90 day) toxicity study was done in a different strain of rats with much lower doses (in feed) to assess safety for the food additive industry [48]. Although this study was not a carcinogenicity study as that requires 2-years of dosing in two species, it is relevant that the authors also concluded the results “were indicative of target organ toxicity pattern that at higher intake levels, such as those tested in the NTP studies, produces more severe toxicity and leads to associated neoplastic lesions.” The amounts of ß-Myrcene used in food additives are orders-of-magnitude lower than those neighbors are exposed to from breathing cannabis emissions (Appendix). Other effects of ß-Myrcene in animal testing include developmental [46] and reproductive toxicities [47] in rats at slightly higher doses, and sedative-hypnotic activity in mice [54].

All the animal toxicity studies were done with ß-Myrcene dosed orally. As detailed in the Appendix (p11), oral dosing results in ~3-5 times lower uptake than by inhalation [34]. Thus, due to this greater update by inhalation, equivalent toxic levels by inhalation are reached at 3-5 times lower calculated levels as compared to oral dosing (i.e., to expose the body to the same toxic amount).

Toxicity/safety studies in humans with isolated ß-Myrcene have not occurred. Thus, one must rely on animal safety/toxicity data to project safety for humans. Separate from carcinogenicity, liver and kidney toxicity concerns based on animal testing, we found two publications on effects of ß-Mrycene in people, one on cognitive impairment and one on sensitization, both of which are relevant to human safety concerns:

1) As high ß-Myrcene levels in cannabis have been associated with sedation [22], a pilot study was conducted in human volunteers tested with a driving simulator [55]. Ingestion of isolated ß-Myrcene in people showed significant impairment of driving-related skills (double-blind, placebo-controlled crossover study). 2) ß-Myrcene was determined to be the sensitizing agent in respiratory hypersensitivity in a brewery inspector [8].

Furthermore, inhalation provides a direct route to the brain via the olfactory pathway [50, 51], resulting in much higher drug levels in the brain than from oral delivery. No animal toxicity/safety studies have been conducted using the inhalation delivery route for ß-Myrcene; unknown brain toxicities may exist.

In 2015,California listed ß-Myrcene under Proposition 65 as a compound known to cause cancer, concluding that the cancers formed were relevant to human toxicity [9]. Additionally, the Food and Drug Administration (FDA) removed ß-Myrcene from its list of approved food additives in 2018 [19].3 More recently, we and others have raised additional safety concerns from ß-Myrcene from cannabis cultivation as ß-Myrcene is a terpene present in cultivation emissions from all varietals of cannabis, often as the dominant terpene [1, 18, 40]. ß-Myrcene is also known to be a skin and eye irritant [49].

Our research team employed two accepted methods to project “toxic” and “safe” exposure levels of ß-Myrcene for people living or working near outdoor cannabis cultivation sites, based on animal toxicity and carcinogenicity data. These are detailed in the Appendix and summarized below.

B. Calculating Projected Toxic and Safe Levels of ß-Myrcene

Method 1 (Appendix Part B): Using well-accepted factors employed by the pharmaceutical industry to convert rodent dosing to human dosing [33], plus accounting for higher bioavailability of inhalation versus oral ingestion of cannabis compounds [34] and predicted accumulation in humans [34, 43], the calculated human-equivalent toxic dose of ß-Myrcene is reached at only 3.5 mg/day for a 15 kg person (e.g., a 33 pound 3-year-old) and at 14 mg/day for a 60 kg person (e.g., a 132 pound adult) (Appendix, Table 2). These doses were calculated as the human-equivalent to the lowest dose tested in mice, which was deemed highly carcinogenic after 2 years of exposure. Toxic effects on kidney and liver were also observed in the 3-month rodent study [3].

ß-Myrcene was carcinogenic at the lowest dose tested in the animal carcinogenicity study; no lower, non-toxic dose was determined [3; footnote 4]. Thus, one must factor in further dose reduction to estimate toxic and safe exposure levels for chronic exposure. The pharmaceutic industry and the FDA understand that even a non-toxic dose in mice or rats may be toxic in humans, and clinical trials typically start at 1/10th or less of the equivalent non-toxic dose in animals. Since no non-toxic dose was determined in the carcinogenicity study, we used 1/10 reduction to estimate a lower “toxic” level of 0.35 mg/day for a small child and 1.4 mg/day for an adult, which at 50% absorption of ß-Myrcene from air gives a projected toxic chronic exposure at ~5 ppb for a small child, and ~20 ppb for an adult. If another 1/10 factor is then used as an estimate of a “safe” level (thus 1/100 of lowest toxic dose tested), this predicts a “safe” exposure level of 0.5 ppb for the child and 2 ppb for the adult.

Method 2 (Appendix Part B)

Another accepted approach for determining safe chronic human exposure levels calculates Occupational Exposure Limit (OEL) of ß-Myrcene in the air using the formula OEL = POD/ (AFc x a x S x MF x V) [42, 44]. Using the rat data, this projects a “safe” exposure level of ß-Myrcene in the air of 2.7 ppb for the child and 10.7 ppb for the adult (Appendix, Table 3).

III. DISCUSSION

Harm to Residents, Workers and Vulnerability of Children People living or working near outdoor cannabis cultivation operations are involuntarily exposed to cannabis emissions including ß-Myrcene on agricultural parcels, in their yards as well as in their homes when vapors enter through windows and doors. They breathe it in 24/7, often for 3-6 months a year. Exposures can continue year after year. Chronic exposure [20] to a compound generally causes toxicity at much lower doses than observed for acute exposure. The quantity of ß-Myrcene inhaled by neighbors (which is similar for children and adults) can be calculated (Appendix Part A, Table 1) and compared to the projected toxic levels (Appendix Part B, Tables 2 and 4). As shown in Table 4B, at 100 ppb, projected toxic doses are reached for children after only 3 months exposure, and for adults after 12 months exposure. Even at ambient levels of only 10 ppb, which is below the level of odor detection for most people [21], the amount of ß-Myrcene absorbed in 6 months per year over a 5-year period is at the projected toxic dose for children (Appendix, Table 4A) and approaches the projected toxic levels for adults by 10 years. For outdoor cultivation sites with two harvests per year, cumulative exposure of 60 grams ß-Myrcene occurs after 10 years at 1000 ppb, which is 50 times the projected toxic dose for adults (Safety Margin 0.02), and 200 times the projected toxic dose for children (Safety Margin 0.005), respectively (Table 4C).

Safety Margin is Toxic Dose divided by Inhaled Dose. When the Safety Margin of projected toxic dose to inhaled dose is less than 1, this means that the inhaled dose is greater than projected toxic dose; exposures even at a Safety Margin of 10:1 (i.e., inhaled dose is one-tenth of the toxic dose) can pose health risks.4 Note that this risk is in addition to the known respiratory toxicities that occur from breathing cannabis emissions (ß-Myrcene, which is a known irritant, may be one of the compounds causing this irritation.) If exposures are even higher (e.g., due to proximity, meteorological conditions, grow area and/or several large nearby cultivation areas), the amount inhaled can reach hundreds of grams after several years.

These calculations show that based on ambient levels of ß-Myrcene near outdoor cannabis cultivation sites [21; 42 Fig 3-1, 1 Odor Unit = 20-50 ppb; thus for a 1 acre grow, ave is ~1050 ppb at 100 ft, ~175 ppb at 1000 ft, and ~82 ppb at 2500 ft, with higher ppb levels for larger grows], the total amount of ß-Myrcene that neighbors are involuntarily exposed to is significant (Table 1), may cause toxic effects and ultimately be carcinogenic, with even greater risk for children (Table 4) as well as infants and fetuses in utero.

Furthermore, unlike pharmaceutical drugs that take into account risk-benefit, there is absolutely no therapeutic benefit for neighbors or workers from inhaling ß-Myrcene, only risk. To put this in context, the lower limit of terpene concentration where more than 50 percent of volunteers reported odor detection is between ~20-50 ppb [21, 42 Kram report]. Levels when the odor is strong or close to cultivation fields can be orders of magnitude higher. Uncontrolled emissions from an outdoor cannabis cultivation site (or from an indoor facility if the odors are not properly filtered) can reach hundreds to thousands ppb ß-Myrcene. Exposure levels can be even higher at locations downwind of a cannabis site when flowering plants are mature. Odor masking or neutralizing agents are not effective for outdoor cannabis fields.5

Risk is higher for infants and children due to multiple factors including their lower weight, higher respiratory rates, immature and developing lungs, and greater physical activity as well as the fact that their cells are more rapidly dividing as they are growing. Since children are smaller than adults, the dose of ß-Myrcene in mg/kg body weight is much higher. As such, a lower total dose may be toxic (Appendix, Table 2). This is consistent with the fact that air pollution affects children [25] much more than adults. On average, a 20 kg (44 pound) 5 yr old child inhales 11,664 L/day, [25] similar to but slightly higher than adult inhalation. Yet for the 5 yr-old, pollutants are concentrated over a 3-4 times smaller body mass. Risk is further magnified for infants or with in-utero exposure of developing fetuses. Most low molecular weight and lipophilic compounds cross the placenta [15], and ß-Myrcene is both low molecular weight and very lipophilic [28]. Cannabis can cross the placenta [26, 53] and can cause low birth weight and neurocognitive deficits [27]. As the projected toxic dose level of ß-Myrcene in cannabis is calculated in mg/kg body weight, the dose experienced by the mother is magnified manyfold in the tiny fetus. Toxicity and carcinogenicity are increased by exposure over a multi-year period. As the rodent studies confirmed, longer exposure times to ß-Myrcene increased toxicity in various organs, long before full-blown cancers appeared.

This paper is not intended to address safety or health effects from ingesting or smoking cannabis. Interested readers are referred to a recent review [52] concerning therapeutic use of cannabis and cannabinoids as well as a review of health risks. The authors concluded “Evidence is insufficient for the use of cannabis or cannabinoids for most medical indications.” They also referenced many studies showing health harms from ingesting or inhaling cannabis including cardiovascular, pulmonary, neurocognitive and psychiatric risks and fetal risks from use in pregnancy [52, and Table 4 in 52].

IV. CONCLUSIONS AND POLICY RECOMMENDATION

This report summarizes known respiratory harms caused to workers, customers as well as residents near outdoor cannabis cultivation fields. It also addresses that ß-Myrcene, a carcinogen listed on California’s Proposition 65, may reach levels in people from breathing cannabis emissions that are equivalent to those confirmed carcinogenic in animals. Children are known to be particularly vulnerable to respiratory and lung damage from air pollutants and may be exposed to toxic levels of ß-Myrcene from outdoor cannabis cultivation in as little as 3 months. Although the calculations in this report are illustrative and actual levels will vary, they show that neighboring properties are exposed to substantial levels including ß-Myrcene. Due to the known respiratory harm and carcinogenicity risk, these cannabis emissions should be regulated as a serious health threat to humans.

There is no effective way to prevent cannabis emissions from leaving cultivation site premises when grown outdoors; the only mitigation for outdoor cultivation to protect the public from exposure to these toxins is long separation distance that takes into consideration size of the cultivation area, topographic and meteorological conditions. Enclosed cannabis operations including indoor and greenhouse cultivation, drying, and processing facilities must be equipped with sufficient filtration (carbon scrubbers) to remove and prevent all emissions from leaving the structure. As topography and climate conditions affect the distance terpenes travel, quantitative monitoring (e.g., gas chromatography) should be required at parcel line to confirm no terpenes leave the cannabis operation’s parcel.

Cannabis cultivation represents a public health threat to residents, customers and workers6 on neighboring properties when it involuntarily exposes them to breathing unhealthy emissions containing toxins and carcinogens, including ß-Myrcene. Property owners must be able to safely and peacefully enjoy their businesses, yards and homes as is codified in the California Code’s nuisance provisions (CCC § 3479 and HSC 41700).

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APPENDIX - see attached report

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