Miners’ Phthisis, Smoker’s Crisis: A Challenge To Protect The Public

Only 14 states in the United States of America still do not allow growing Cannabis for
medicinal or recreational uses. Only 11 states do not allow recreational or medical use. Hemp is
now allowed in all states, and youthful theft of foliage in misdirected search for euphoric
combustion is not unheard of. Tobacco is allowed both for consumption and growing nationally,
although the growing is predominately only in 7 states. Silicate-containing products are allowed
for crop nutrition and protection for these three crops, despite determination that some forms
of silica cause silicosis when inhaled and eventually lung cancer. Despite strong evidence of this
hazard, neither the federal nor state regulatory systems have acknowledged nor prevented this
dangerous practice. Every agricultural use of these products has alternative options without the
risk, as silicon is not an essential nutrient for any commercial crop in the higher plants. Obvious
empirical testing could settle this issue by demonstrating or not the potential exposure risk from
this failure to regulate in the public interest with the prudent principle placing public health as
higher than allowing continued chancy commerce.
The silicates enter the agricultural arena in many ways; indeed, as the second most
abundant element in the Earth’s crust it would be impossible to contain exposure in the diet and
contact with the surface of the planet. However, even centuries ago physicians recognized that
some workers, especially those working underground and within a few other trades such as
ceramics and stonemasonry had respiratory diseases at a much higher rate than everyone else.
Similarly, the apparent nutritional and pesticidal benefits of supplementing growing plants with
silica-containing inputs were known for nearly a century. These silicates entered as forms of
silicon dioxide (SiO2), sodium or potassium silicates or metasilicates, silicic acids and their salts,
and possibly as numerous synthetic organosilicate adjuvants used as spreaders for other crop
inputs. Only a very small set of three crops are potentially affected by the accidental conditions
that combust these inputs for inhalation, and the many beneficial properties offered by silica in
these three crops can be reproduced in all cases by alternative inputs. Industrial hazards from
burning the crops with the highest endogenous silica content, those being rice and sugarcane,
have been well known for almost half a century. In all cases, silicates exiting the agricultural arena
in the form of smoke are dangerous.
This author, who has been working in agricultural pesticides for over three decades,
became aware of this potential problem only recently while reading a publication concerning
protection product evaluations on Cannabis. A silica-containing product is being used in Canada
and several in the United States, so I recently informed toxicologists and regulators at the
California Department of Public Health (CDPH), California’s Department of Cannabis Control
(DCC) and the California Department of Pesticide Regulation (DPR) of my concern. Their response
to date has been to acknowledge that their regulatory decisions allowing these suspect uses are
based upon prior evaluations done by the United States Department of Agriculture (USDA), the
United States Food and Drug Administration (FDA), and the Environmental Protection Agency
(EPA). They revealed no actual studies conducted by the DPR, CDPH, or DCC, and this author has
found no actual studies conducted by the FDA, USDA, nor EPA, in-house, although the latter
commissioned four small assays from a nearby pesticide manufacturer.
The evolving science surrounding silicosis and the corresponding legislation, or lack
thereof, follows, categorized chronologically under the null hypotheses disproven along the way.
The chain of disproven hypotheses raising concern is not exactly chronological, nor exactly
logically sequential, but stated to explain the current dilemma in a chronological fashion.

HØ: Silica dust is not correlated with excess proportions of the human population
exposed to higher amounts of these substances due to occupational exposure of inhaled dust
presenting with lung maladies described variously as respiratory diseases, phthisis, fibrosis,
pneumoconiosis, silicosis, and lung cancer, but distinct from tuberculosis.

HØ: Silica dust association with silicosis does not only present in humans with chronic
exposure to inhaled dust.

“If any one man more than another stands out as the father of the modern conception of
silicosis, it is the late Professor J. S. Haldane, whose able investigations into dust hazards are
summarised in the Second Report of the Royal Commission on Metalliferous Mines and Quarries,
1914, (Haldane 1914). To this obscure publication the better known and widely quoted Milroy
Lectures of Collis, 1915, (Collis 1915) appear to owe their inspiration. Much of the epidemiological
spade work with respect to silicosis which is commonly attributed nowadays to others may be
traced to Haldane. The gist of Haldane’s thesis was “If in any class a high death-rate from
pulmonary tuberculosis is found occurring at a later period of life than is usual for pulmonary
tuberculosis and if this high death-rate is associated with a high death-rate from other respiratory
diseases, then this class is exposed to the inhalation of injurious dust.” The one factor which
seemed to be common to all the injurious dusts was silica; therefore the Report concludes “The
cause of miners’ phthisis is the inhalation of dust of crystalline silica, upon which is superimposed
tubercular infection.”
Thus, the industrial hazards of siliceous dust first became apparent by virtue of an excessive
incidence of pulmonary tuberculosis amongst the affected peoples. To this day, tuberculosis is
perhaps still the best index of a harmful dust (Kettle 1934).
Silicosis may be defined as an industrial or occupational disease of the lungs, sporadic in
incidence, insidious in onset, of great chronicity, occurring amongst workers who are exposed for
years to the inhalation of siliceous dust. It is characterised essentially by extensive nodular fibrosis
and by a marked tendency on the part of its victims to die eventually of pulmonary tuberculosis.
“I believe the disease is the same all over the world,” said Haldane (Haldane 1914) and most other
authorities support this view.” (King and Belt, 1938)

“Although the term pneumoconiosis was not introduced until the nineteenth century, clinical
symptoms were naturally enough associated with the inhalation of dust in occupation by the
earliest medical writers. In the Renaissance both physicians and mining engineers were well aware
of the fact that the metal miner suffered from shortness of breath and died prematurely, and
anatomists had described "heaps of sand" in the lungs of stone cutters which grated on their
knives. They called the condition phthisis, their term for any chronic disease of the lungs which
was associated with emaciation and expectoration. While most of the various conditions originally
known by this name were differentiated and fully described in the eighteenth and nineteenth
centuries, it was not until 1902 that the role of inhaled dust began to be understood. In that year
an English departmental committee, of which Dr. J. S. Haldane was the outstanding member,
pointed out that the phthisis from which the Cornish tin miners suffered was different from
ordinary tuberculosis. They concluded that "the primary injury of the lungs is due solely to the
inhalation of stone dust but that this injury, while it is apparently capable of gradually producing
by itself great impairment of respiratory functions … also predisposes enormously to tuberculosis
of the lungs, so that a large proportion of the miners die from tubercular phthisis."
A few years later, in 1915, Collis(Collis 1938) demonstrated that not all kinds of dust had the
same effect.; His statistical analyses of morbidity and mortality in workmen in various dusty trades
 indicated most clearly that exposure only to free silica dust was particularly dangerous.” (Gardner
1938)
The causal link of silica to lung disease was suspected by epidemiological study over a
century ago, and the advances in pathological study made a very strong case by 1938, when the
above passages appeared. The author has added underlined emphasis to alert the reader to the
over 80-year-old determination of the chronic nature of the malady having a siliceous etiology.

HØ: Silica dusts are not ubiquitous in nature and dietary exposure is therefore
controllable.

In 1973, the Joint Food and Agriculture Organization of the United Nations/World Health
Organization (FAO/WHO) Expert Committee on Food Additives pronounced the Average Daily
Intake (ADI) of SiO2, used as an anti-caking additive, was
“not limited” (FAO/WHO, 1973)

HØ: Silicosis pathology in humans is the same as in animal models.

By 1975, an excellent review of the evolving state of pathology and our increased
understanding afforded by those advances was included in Rigdon and Grasso where the miner’s
phthisis was by then accepted as the silica etiological agent causing pneumoconiosis, which was
by then recognized as also being caused by the etiological agents coal dust and asbestos as well.
Histopathological differences in numerous studies reviewed lead the authors to conclude
“…a different pathogenesis in man and in the rat.” (Rigdon and Grasso 1975).

1977 and 1978 brought the issues of silicates, smoke, Cannabis, paraquat, and rice into a
swirl of public attention for Californians. The Federal Clean Air Act Amendments of 1977, to be
implemented by the EPA, required that all National Ambient Air Quality Standards (NAAQS) be
attained by 1982. California rice growers burned their fields, and the public was becoming
concerned by the pollution and potential health risk, if not the fact that the California officials
were not enforcing these standards, yet, because the rice straw burning was the leading cause
of not meeting those standards and the rice industry was a significant segment of the economy.
The high content of SiO2 in rice straw made it tougher and more difficult to till under, requiring
more passes with diesel-burning equipment than a field of wheat or tomato following harvest.
The silica slowed the rice straw’s decomposition, leading to toxic gas formation that damaged
the next crop’s seedlings, and incorporation cost dramatically more than burning, which was the
main practice for preventing build-up of the soil- and straw-borne pathogen causing rice stem
rot, the most significant disease of rice in California at that time. The proven silicosis risks from
industrial sources and suspected contributions burning of this straw might add to respiratory
disease for Californians were known to California scientists and physicians, if not addressed as
vocally as the more well-known respiratory risks associated with the smoke’s particulate matter
and recognized gaseous pollutants, such as the various nitrogen and carbon oxides. Calls for
banning the practice were heard.
As if to add spice to this stewing turmoil, the 1978 revelation by the federal government
that they had been for several years supporting the Mexican government’s efforts to apply
paraquat to Cannabis (and opium, Papaver somniferum) fields, and that some intercepted
contraband had tested positive for this dangerous additive, set off a panic in Californians, the
main market for these exported flowers. Conscientious California laboratory owners stepped in
where the state and federal government failed and offered anonymous testing for this herbicide,
providing Californians with some sense of safety when confronted by federal administration
bureaucratic action at odds with the recommendations of their own scientists who lobbied for
safer herbicide choices. Californians very vocally alerted the world they were very concerned with
anything being put on their favorite state flower of commerce.

In 1978, The PQ corporation, manufacturers of potassium silicate, submitted their own

written statement in lieu of an oral hearing presentation to the Select Committee of GRAS
(“Generally Recognized As Safe”) Substances who were providing an independent evaluation of
the safety of certain silicates when used in foods, at the behest of the FDA. At that point in time,
SiO2 was not actually in much, mostly as a substance migrating to foods from paper and
paperboard packaging materials, and regulated separately for use as an anticaking agent, a
stabilizer in beer production, and an adsorbent for dl-tocopherol acetate and pantothenyl alcohol
in tableted foods for special dietary use [21 CFR 172.480]. Looking at all potential sources, the
committee even tallied the residues contributed by filtering through diatomaceous earth (DE) for
many fluids. Non-dietary sources were considered, but with little focus upon other routes of
delivery. The GRAS approval for the FDA came through, but not without this caveat:
“The Select Committee is aware of the extensive literature on the potential toxicity of inspired
silicate particles. In addition, fibrous nodular lesions in the peritoneum caused by talc dust from
surgical gloves and the intentional use of talc to induce adhesions of the visceral and parietal
surfaces of the pleural cavities in treating pneumothorax are well documented examples of the
tissue reactions to talc as a foreign material. Pneumoconiosis from chronic inhalation of silicate
dust represents a similar tissue response. The pathological changes in reactions to silicates have
recently been reviewed (Rigdon and Grasso 1975). The postulated relationships between
mesothelial cell proliferation in response to silicates and chronic exposure to asbestos particles
and the development of lung neoplasms (which is assumed to involve a lag period of 15 to 20 yr)
remain controversial; however, the chronic inflammatory reaction to silicates is not disputed.”
(FDA 1979)
The underlined emphasis is added to alert the reader to the preponderance of pathology
supporting the dangers of inhalation of silicates by 1979 as well as acknowledgement of the lag-
time issue in addressing effects and the nature of the maladies associated with inhalation to be
chronic, not just acute. More recent focus upon the time-lag involved has shortened this interval.
One study, trying to tease the excess lung cancer mortality risk posed by inhaling crystalline silica
dust followed over 2300 DE miners over 45 years. DE is an amorphous form of SiO2, but the
miners are exposed to crystalline forms in obtaining ore (about 1% quartz), and more
concentrated forms (10%-25% cristobalite) in its’ processing. The location studied, Lompoc, CA,
had excellent dust monitoring records from 1948. The United States Occupational Safety and
Health Administration (OSHA) wasn’t created until 1971.
“Unlagged and lagged (2, 5, 8, 10, 12, and 15 year periods) cumulative exposures were
considered. … Exposure to respirable crystalline silica dust was a significant predictor (p<0.05) in
nearly all of the models evaluated and the linear relative rate model with a 10 year exposure lag
seemed to give the best fit in the Poisson regression analysis.” (Rice et al. 2001)
 1980 saw the threat of a rice burning ban acknowledged at the University (Nelson et al.
1980) and commodity group level, a proven strategy to delay legislative address affecting
growers’ bottom lines. The California Rice Research Board began funding research into
alternatives to burning, and lobbyists managed to work toward waivers from the NAAQS in these
“non-attainment” areas. In fact, the stall would work to prevent the ban to most rice burning
from even beginning until 1991 (Connelly et al. 1991), and then only following a long phase out,
adding even more time to the clock, and resulting in a final allowance by 2001 of 25% of the
historically burned acreage (125,000 of the half million acres) to still be flamed in the late
autumn.

HØ: The pathology of inhaled silica dusts is the same for crystalline and amorphous
forms of SiO2.

HØ: There is not sufficient evidence from animal exposure studies to conclude crystalline
SiO2 is carcinogenic.

HØ: There is not limited evidence from animal exposure studies to conclude crystalline
SiO2 is carcinogenic.

HØ: There is not a preponderance of epidemiological and case-controlled human

exposure clinical studies to support the causal link between chronic exposure to inhaled
crystalline SiO2 and the development of lung cancer.

Pathologists still had not nailed down the exact pathogenesis of silica and respiratory
distress but worked hard to validate safety parameters to mitigate this problem for miners and
other workers. Some trends were emerging from the data, namely that the silicates of concern
were mostly from the crystalline, rather than amorphous forms of the various silicates. This freed
some efforts focused upon DE and other non-crystalline forms to be directed more toward the
suspect offenders.
The World Health Organization’s International Agency for Research on Cancer (IARC)
published its’ first monograph on silica and some silicates in 1987, adding several hundred new
pathology and epidemiology studies since Rigdon and Grasso’s 1975 review mentioned above,
and concluding there was sufficient animal data and limited (one report shy of sufficient) human
data to establish crystalline silica as carcinogenic; their criteria being
“Sufficient evidence is provided by at least three positive entries, one of which must involve
mammalian cells in vitro or in vivo and which must include at least two of three end-points - DNA
damage, mutation and chromosomal effects” (IARC 1987).
This marks one of the earlier examples of the EPA refusing to acknowledge the findings (still,
today!) of the IARC, and completely ignoring the several hundred peer-reviewed studies cited in
the IARC’s comprehensive work (and periodic updates, see references to follow); a trend carried
on throughout the decades, as recently chronicled with respect to the glyphosate regulatory
wars. (Benbrook 2019)
“Glyphosate is probably carcinogenic to humans (Group 2A).” (IARC 2017).
This author hopes the California DPR continues with its’ historically higher bar for regulation
prioritizing public health concern, restricting some more egregious pesticides to a greater extent
than the EPA.
1991 was the EPA’s Reregistration and Eligibility Document (RED) for SiO2 and Silica Gel,
in which, while acknowledging a single report of tumorigenic evidence from an inhalation study
in rats from 1940, and “diffuse tissue reactions” in rabbits from a single study in 1954, both long-
term, chronic investigations of 200-800 days for the rats and 1100 days for the rabbits (and both
using amorphous silica, specifically DE, and acknowledged by the EPA as sourced from the IARC’s
1987 report, which gave hundreds of studies more recent), stated in their “Human Health Risk
Assessment” that since the FDA had determined these substances as GRAS (FDA 1979), the
“…EPA believes based on the use patterns, the application is infrequent and therefore
exposure is acute rather than chronic. In addition, the labels caution the applicator to avoid contact
with eyes and skin, avoid breathing dust, and use a dust mask for prolonged periods of use. Given
these factors and assumptions, EPA concludes the human health risk is low and not unreasonable.”
(EPA 1991).
Interestingly, the EPA conducted no studies themselves to come to their decision. They apparently
commissioned a nearby pesticide manufacturer, Fairfield America Corp., to conduct a single acute
dermal, a single acute inhalation, and a single primary eye irritation and a single primary
inhalation study, from which four studies only the EPA’s determination of what category of
toxicity the results led them to assign to tested materials, only identified as silica gel for the first
two (acute dermal, acute inhalation) but not for the others. These reports were not included in
the appendices to the RED and are unavailable. There is no way to view any details. One might
say that this might have been less than forthcoming upon the part of the EPA. To commission an
acute inhalation study using silica gel (an indurated formulation of amorphous SiO2), at a point in
time when all evidence was pointing to the inhalation toxicity of SiO2 as associated with the
crystalline forms, and not to test the drier, dusty, DE form of SiO2, was a choice, providing a single
acute inhalation toxicity study for this RED to satisfy the minimum for the silica gel inclusion in
the RED decision, as the SiO2 was covered by reference to the single chronic inhalation study of
fifty one years prior, referenced above. This RED document approves SiO2 for use as an acaricide
and/or insecticide for many crops, including tobacco. The acute inhalation toxicity studies citing
evidence for their namesake for most crystalline forms cited in the IARC report of four years prior
went unacknowledged. To their credit, the reregistration decision restricted the source material
to DE, an amorphous form of SiO2, and the only studies cited on amorphous inhalation in the
IARC data, the 1940 and 1952 studies noted above. The EPA did not include the IARC note
attached to the 1940 entry:
“(The Working Group noted the inadequate description of the exposures.)” (IARC 1987, with
reference to Campbell 1940)
Similarly, the tobacco industry might have submitted acute inhalation studies showing no
carcinogenic effects from rats who smoked a single package of cigarettes.

HØ: Synergistic interactions are not important in carcinogenesis.

HØ: Co-exposure to radiation associated with radon gas in underground mines and
chronic inhalation of crystalline SiO2 dusts does not affect the incidence nor decrease the
timeline of tumorigenesis in rats.
 Pathologists kept working to define the highly suspected carcinogenicity (already proven
to those of us who put health before commerce) for SiO2, and to account for any confounding
factors preventing unassailable ‘proof’. Given the long association of miners with the phthisis, a
study to investigate the interaction of radiation was published in 1992.
“THE EXCESS of lung cancer in underground miners is closely related to the elevated exposure
of alpha-emitting 222Rn gas and its alpha-emitting decay products (review by Samet and Hornung
1990)” (Spiethoff et al. 1992).
The authors combined the chronic inhalation study using crystalline quartz well known to cause
lung tumors in rats, with the radiocontrast agent Thorotrast (232ThO2) unwisely administered to
millions throughout the 1940s and 1950s, where it remained in their organs. The 22-year half-life
caused these patients to emit harmful alpha radiation for the rest of their lives. It found use in
this study as a proxy for the environment of underground miners, where radon accumulates and
also contributes to lung cancer. The significant increase of the lung tumor risk they found, and
marked shortening of latency times (first lung tumor was found 1 y after treatment) and a higher
total incidence of these tumors led to their conclusion
“Our study shows a significant interaction between quartz and Thorotrast (exhalation of 220Rn)
in the induction of lung cancer. It proves that the effects of radiation can be strongly influenced by
other agents. With regard to the evaluation of risk factors for the general population, which is
always exposed to a variety of physical and chemical agents including environmental 222Rn, the
results emphasize the importance of synergistic interactions in carcinogenesis.” (Spiethoff et al.
1992).

HØ: Regulatory limits established to protect workers chronically exposed to inhaled

dusts of crystalline SiO2 are below any levels established as safe in animal models.

More evidence accumulated from rat studies, already deemed sufficient in 1987 by the
IARC, with new twists found by closer scrutiny and improved assays. In 1995, a chronic crystalline
silica exposure at much lower levels than previously determined as sufficient for protecting
workers and below many regulatory limits (see IARC 1987, pages 48-49 for global comparisons of
those limits in 1987), found numerous tumors (cancers), and reaffirmed the lack of findings for
the same from any studies using hamsters or mice. (Muhle et al. 1995).

HØ: Heating rice husk ash (RHA) does not release crystalline SiO2 that causes respiratory
damage in rats.

HØ: Workers in the RHA industry chronically exposed do not present with clinical
silicosis at an elevated rate compared to the population at large.

HØ: Heating RHA, a combustive and pyrolytic practice, does not mineralize endogenous
silicic acids (polysilicic acid) of the Oryza sativa in a predictable pattern that correlates with
heating temperature to forms of increasing crystalline SiO2 content with increasing
temperature.
 HØ: Indications of severity of respiratory damage in rats exposed to RHA do not
correlate with crystalline SiO2 content in the RHA.

The next year, 1996, the link was finally made to show the extreme danger posed by
burning rice (Liu et al. 1996). Rice husk ash (RHA) is an agricultural byproduct of commercial
significance. It is made by burning the rice hulls. It is sold as an additive in many industries, but
especially cement, where its’ finer grain makes a stronger cement. Careful study found the kilning
temperatures associated with various crystalline rearrangements of the silica within the hulls and
matched them to rat silicosis damage. The authors also traced affected workers with
epidemiology confirmed with radiology, did various histological investigations, and determined
free silica content associated with the various temperatures at which the husks were ashed. They
found an increase in crystalline silica content as the temperature of kilning increased, and the
higher silica contents administered to the rats had more pathological markers of silicosis.
“The component analysis of rice husk showed that the silicon in rice husk exists in the form of
polysilicic acid(Zou 1976). The rice husk which contained a great deal of polysilicic acid only induced
local dust cells, and foreign body granuloma of the rats which were exposed to rice husk dust for
twelve months. No change in pulmonary fibrosis was found in the exposed rats. Therefore, the
form of silica was closely related to pulmonary fibrosis(Garder 1938, King 1953). The experiments proved
that when polysilicic acid in rice husk was heated, both the crystalline silica and the crystalline form
of silica in if were changed. The polysilicic acid in rice husk was non-crystalline silica. As the
treatment temperature rose, the non-crystalline silica became crystalline and the amount of
crystalline silica gradually increased, and in the crystalline state of silica, quartz became tridymite
and cristobalite. When rice husk was treated at 1,300 °C, the free silica content was 93.8% in which
cristobalite was 38.0% and tridymite 6.1%. RHA at 1,300 °C became the inorganic dust which
mainly consisted of crystalline silica, and crystalline silica caoused diffuse lung fibrosis and silicotic
nodules. (Liu et al. 1996).
The underlining and italicization are this author’s. The spelling and typographical errors are
courtesy of the Journal of Occupational Health. These findings are of great importance, because
silica in plants is almost all found in the form of silicic acids. Topical or drench applications of any
silicate nutrient or pest control product will be absorbed in this form, and rapidly. The pyrolysis
of these husks converted the silicic acids into crystalline forms of SiO2. It would not be a leap to
hypothesize that Cannabis shares silica metabolism patterns with Oryza.

HØ: There is not sufficient evidence to conclude inhaled crystalline SiO2 is carcinogenic.

The next year was the decade revisit of the IARC to the silica questions. The 1997 review
(IARC 1997) added well over one hundred new studies since the 1987 report and concluded there
was sufficient evidence that crystalIine silica (inhaled in the form of quartz or cristobalite from
occupational sources) was carcinogenic in humans. Their new evaluations gave numbers to the
categories. Carcinogenic substances were to be known as category 1. This would be copied by
most regulatory agencies.
The following year, 1998, the EPA published its’ guidelines for both the Acute Inhalation
Toxicity (OPPTS 870.1300) (EPA 1998a) and the 90-Day Inhalation (OPPTS 870.3465) (EPA 1998b)
Toxicity Health Effects Tests. By the very nature of the testing, the longer test,
 “…is not capable of determining those effects that have a long latency period for development
(e.g., carcinogenicity and life shortening). Extrapolation from the results of this study to humans is
valid only to a limited degree.” (EPA 1998b)
To revisit and test all the chemicals already approved, even those with overwhelming data
demonstrating respiratory damage, was obviously beyond the capacity of the EPA.
Pathological assay advances in the war on cancer were proceeding rapidly in the last
decades of the 20th century, and shades of cell death or proliferation were more finely defined
as markers of cancerous progression or non-carcinogenic pathologies, as if the latter were
somehow less devasting to the victims. By 1995, the
“Chronic lung lesions induced by crystalline silica in rat represent a model for studying the
interaction of fibrogenesis, epithelial hyperplasia, and carcinogenesis.” (Williams and Saffiotti
1995).
and the researchers in this case were refining this model system by discoveries focused upon the
role of TGF-β1 interacting with the other two factors. In the silica-related respiratory maladies,
the improved techniques were focused upon these distinctions, to aid understanding between
the differing pathological endpoints of inhalation of SiO2 dusts depending on their crystalline or
amorphous forms. Aiming to understand if chronic inflammation was of itself a predisposing
factor to a carcinogenic progression, a closer look in rats reported in 2000 showed the difficulty
still to make this call. Apoptotic result from the amorphous irritant to a much greater extent than
the crystalline aggravation led one research team to report that
“…inflammatory cell response after subchronic exposure to both types of silica, suggests that
in addition to inflammatory response, particle biopersistence, solubility, and direct or indirect
epithelial cell cytotoxicity may be key factors for the induction of either mutagenic events or target
cell death.” (Johnson et al. 2000)
Other groups focused upon other factors; the tumor suppressor gene (Liu et al. 2000) and its’
interaction with stress (Ishihara et al. 2002), and the natural killer cells (Ishihara et al., 2001).

HØ: Topical or soil drench nutritional supplements of potassium silicate (or sodium
silicate) in aqueous carrier are not absorbed into plants as silicic acid.

In 2002, The PQ corporation petitioned the National Organic Program (NOP) of the USDA
to determine if potassium silicate might be used in the federally recognized ‘organic’ farming
(USDA 2002). In 2003 the National Organic Standards Board (NOSB) did not approve the petition,
then, but noted
“Applications of potassium silicate pose a risk primarily from inhalation or ingestion of silica-
rich compounds. Respiratory problems in the agricultural sector due to inhaled dust are a proven
concern (Schenker 2000). Decades ago, it was shown that dust arising from storage and handling
of wheat grains contained particles that were believed to cause respiratory ailments (Baker 1961).
Burning of high-silica crops, such as rice and sugarcane, have been problematic for worker health
in the past (Boeniger et al. 1988). There is also significant indirect evidence linking ingested plant
silica and human cancer (Sangster et al. 1983, Bhatt et al. 1984, Hodson et al. 1994), but there
currently is no connection between plant silica and inorganic silica sources. Mitigation of health
risks associated with respiration of silica-laden dust can be achieved though proper use of personal
protective equipment including a NIOSH-approved dust respirator where dust occurs.” (USDA
2003).
And earlier in the same report they revealed a knowledge of the silicon geochemical cycle they
still fail to incorporate into regulatory policies
 “Diluted potassium silicate solution readily depolymerizes into various silica-based
species loosely associated with potassium ions. Concentrations used in foliar sprays and nutrient
solutions are dominated by silicic acid, which is readily absorbed by plants.” (USDA 2003).

HØ: Nutritional supplements of potassium silicate (or sodium silicate) are not absorbed
into plants at a level that can be detected above their background level.

In 2004, trying root feeding to stem off powdery mildew disease, which works, Kanto et
al. fed hydroponic strawberries potassium silicate.
“…only the silicate content differed markedly between the control and treated plants. … The
maximum silicate content was about 24 times that of the control. (Kanto et al. 2004)
Nobody smokes strawberries, but when PQ Corporation petitioned the EPA for an exemption
from a residue tolerance for potassium silicate the next year in 2005, part of their basis for the
request was the null hypothesis stated before this paragraph, and when the EPA awarded that
exemption a year later in 2006, they apparently had not read this study either. See two
paragraphs below.

HØ: Cannabis does not accumulate SiO2.

Without going into an exhaustive explanation of the silicon geochemical cycle, and why
this author does not refer to it as the biogeochemical cycle (see Exley 2015), the amorphous
forms of SiO2 deposited within plants, or reconstituted from the silicic acids deposited within
their tissues or upon their surfaces, accumulate in rice, and also, Cannabis. (Dayanandan and
Kaufman 1976, Guerriero et al. 2019).
In 2005, PQ Corporation petitioned the EPA, this time to exempt potassium silicate from
the setting of a residue tolerance, thereby making it an “exempt” pesticide. Their reasoning was
not without basis.
“Since both potassium and silicic acid are rapidly absorbed and utilized by plants, it is not
possible to detect residues of potassium silicate applied as an insecticide essentially 24 hours after
application. Silicates such as potassium silicate are not discernable from silicates found
ubiquitously within crops and the environment in general. Further given the significant percentage
of crop tissues that contain silicon dioxide, it is unlikely that any significant increase in silica
concentration due to silicate pesticide applications would occur.” (EPA 2005).
Again, as during the RED for SiO2 in 1991 when continued use on tobacco was overlooked, nobody
seems to have considered inhalation of a smoked agricultural product as a possible route of
exposure.
In 2006, PQ Corporation again petitioned the USDA NOSB, this time for aqueous
formulations of potassium silicate (USDA 2006), and in a favorable decision from the EPA,
received their exemption from a residue tolerance (EPA 2006). Meanwhile, another research
team was unraveling the pathological contributions of nitric oxide and reactive oxygen species in
the rat silica inhalation model system for cancer research (Porter et al. 2006).
The USDA NOSB did not approve potassium silicate for the NOP (USDA 2007). However,
the EPA issued their BIOPESTICIDES REGISTRATION ACTION DOCUMENT which required PQ
corporation to do nothing more for this rebranding from pesticide to ‘biopesticide’
“…since the product is being registered after November 1984 and is, therefore, not subject to
reregistration.” (EPA 2007)
Another interesting revelation in this same document was the passage
“Potassium silicate is used as a non-food use inert, but does not a have a tolerance exemption
as an inert ingredient.” (EPA 2007)
which, while not identifying which products’ proprietary formulations revealed to the EPA but
protected from public disclosure potassium silicate is used in as an inert ingredient, reveals that
potential exposure might extend far beyond just the products listing potassium silicate. Aside
from the inhalation risk associated with the closely related and possible modification of the
product, crystalline SiO2, potassium silicate is an excellent pesticide and nutritional supplement
and has many other safe uses, of which only one other might be of concern: as a binder in the
making of charcoal briquets.

HØ: The potential inhalation of crystalline SiO2 evolved and released from pyrolyzed
amorphous forms and/or silicic acids in or on a Cannabis flower on a chronic basis does not
occur at a measurable level.

The first related clinical cases found by this author involving Cannabis smoking and SiO2-
induced respiratory distress were reported together in France in 2009 (Delourme et al. 2009).
Sand, a mixture of crystalline and amorphous forms of SiO2, and glass microbeads, an amorphous
form, were being used to adulterate flowers to add weight and to make the Cannabis appear to
glisten as if they had more beads of resin containing desirable cannabinoids. The first patient was
admitted for an acute inhalation pneumonitis secondary to smoking Cannabis with sand, and the
second presented with bleeding from the back of the nose, throat and mouth, painful breathing,
and burning chest pain. The first patient showed ground-glass opacities on a computed
tomography (CT) scan, but the second did not. However, the glass microbeads were found in the
Cannabis sample with simple microscopy.

HØ: Lighter flames do not reach temperatures high enough to initiate amorphous forms
of SiO2 to transition to crystalline forms.

Apparently unaware of the work of Liu et al. 1996, Le Blonde et al. 2010 confirmed the
earlier work in the other major crop with high silica that is regularly burned: sugarcane. Again,
the conversion of amorphous forms of silicon in plants to crystalline forms in the ash followed
predictable patterns of increasing content with increasing temperature. The ‘trash ash’ of the
field-burning of foliage didn’t reach high enough temperatures for long enough to significantly
release crystalline forms, but the ‘bagasse ash’ of commerce (similar to RHA in uses) recovered
from the processing for sugar was very high in crystalline SiO2 content at boiler temperatures of
only 700-900 °C.
The literature values vary for flames from matches (surprisingly higher than disposable
butane lighters) to modern torch lighters (very high temperature) and even more modern plasma
lighters (among the very low temperature options) but most are sufficient to cross the
transitional ranges recorded (also somewhat variable by reference) for amorphous to crystalline
SiO2, which spans through various crystalline forms over roughly 550 to 1300 °C. For quick
reference, the torch lighters are, for the rest of the world outside of the United States, 1371 °C.
Using the U. S. Transportation Security Administration (TSA) as a reference,
 “Torch Lighters
Carry On Bags: No
Checked Bags: No
Torch lighters create a thin, needle-like flame that is hotter (reaching 2,500 F) and more
intense than those from common lighters. Torch lighters are often used for pipes and cigars, and
maintain a consistent stream of air-propelled fire regardless of the angle at which it is held.” (TSA
2023)

The IARC met again in 2009 but did release their third report until 2012 (IARC 2012). This
confirms and refines the proof they found for human carcinogenicity due to inhaling crystalline
silicon dust as “limited” in 1987 (though already sufficient in animals), “sufficient” by 1997, and
still sufficient 15 years later. Well over a hundred newer, more sophisticated assays and carefully
controlled studies are referenced, bringing the total peer-reviewed science focusing upon this
danger of silicosis and cancer reviewed by the IARC to over three hundred articles spanning over
80 years.
It is with some irony that the 2014 Technical Evaluation Report (USDA 2014) Compiled by
the USDA Agricultural Marketing Service (AMS) Agricultural Analytics Division for the USDA NOP
to include Aqueous Potassium Silicate claims
“FDA has concluded that potassium silicate represents no hazard to the public.”
citing the 1979 report (FDA 1979). There is no mention of the inhalation toxicity caveat quoted
therein (see passage quoted above), and further mentions of inhalation toxicity are based upon
the registrants’ submitted acute inhalation data; that is, data submitted by PQ Corporation for
their petition in 2006 and commissioned by the EPA from the pesticide manufacturer Fairfield
America Corp. in 1991, not any studies conducted by the GRAS committee, the FDA, nor the EPA.
In 2018, Borm et al. (Borm et al. 2018) reviewed the state of genotoxicity validation for
crystalline silica in the lungs. Good evidence was somewhat equivocal at the IARC 1997 report,
but strong enough to note. The exact mechanism is still unanswered, due to in vivo results
differing from in vivo, but the researchers focusing the closest on this issue now favor a secondary
genotoxicity model in vivo.
While it is the policy of the FDA and the EPA and the USDA NOP that the registrant or
petitioner is responsible for obtaining the data submitted, the choice to accept these studies at
face value, without allowing the public access to review that data short of FOIA procedures, and
to not conduct their own studies to verify or disprove the information they must balance against
what the scientific community is reporting and to simultaneously ignore overwhelming data to
the contrary, is a policy choice. The 1991 RED for SiO2 allowing continued use on tobacco might
have been an oversight, but even if acute and chronic studies hadn’t shown links of amorphous
SiO2 to silicosis, they had certainly shown plenty of evidence of inflammation. And speaking of
inflammation…
2018 also saw a clinical report of three marijuana inhalation injuries
“…in adolescent males, with significant findings of bilateral pulmonary nodules and ground
glass opacities on chest imaging associated with recent marijuana inhalation. Lung biopsies in two
of the three patients confirmed silica-induced pneumoconiosis …”
‘Considering the commonality of cannabis consumption and lack of federal regulations in its
distribution, pneumoconiosis from adulterated marijuana may be more common than is reflected
by current literature.”…
 “Lastly, we did not identify the source of aluminum and/or silica in the two patients with
pneumoconiosis. One hypothesis is aluminum and silica were aerosolized from the coating on a
bong, water pipe, or vaporizer during marijuana inhalation. (McGraw et al. 2018)
These authors’ identify the 2nd of the three patients as
“Patient 2: Silica-induced pneumoconiosis from marijuana “dabbing” (McGraw et al. 2018)
and their discussion covers the extremely few clinical cases of record for marijuana inhalation
injuries proving to be pneumoconiosis from adulterated marijuana. It doesn’t mention the cult
of dabbing ritual, with their preferred quartz ‘dab rigs’. The discussion brings home the clinicians’
difficulty in such diagnoses. Cases of talc adulteration have been recorded, and fungal
contamination, and many cases of other drugs into which Cannabis cigarettes have been dipped
and allowed to dry off. Silicosis is a rarity to think about, requires biopsy to confirm strong
imaging hints from x-ray or CT, and was formerly only considered a possible etiology if patients
were in certain occupations. With illegal Cannabis still prevalent and few customers or physicians
looking for dishonest spiking with microglass beads or sand, or possibly, growers adding
nutritional or crop-protective silicates as the adulterants, the prevalence of silicosis from inhaling
crystalline SiO2 with smoked Cannabis is unknown. It’s when the coughing doesn’t stop.

HØ: People consuming Cannabis by smoking do not use lighters or matches or gas stove
burners to ignite the Cannabis, sometimes scores of times daily for many years.

This author is reaching out for assistance to disprove this null hypothesis:

HØ: The potential inhalation of crystalline SiO2 from smoking Cannabis (or tobacco)
cannot be lessened by preventing the addition of amorphous SiO2 to these commodities.

Can you burn Cannabis (and tobacco) treated with potassium silicate using a smoker's
suite of ignition devices (cool 'plasma' lighters, disposable butane lighters, matches, hot 'torch'
lighters) and characterize the emission, or not, of any crystalline hazards, such as tridymite or
cristobalite? I suspect filter-capture from smoke is possible. With all the existing toxicology data
available, this missing data might carry the most weight.

This author lacks these resources, or would not be reaching out. I have begun contacting
leading researchers asking for their help, including the California DPR, but was told that they
would “discuss with our team internally but understand that DPR does not perform this type of scientific research.”
(personal communication).

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