In this case-control study of marijuana smokers, nonsmokers, and tobacco-only smokers, smoking marijuana was associated with paraseptal emphysema, bronchiectasis, bronchial wall thickening, and airway mucoid impaction.
■ In this retrospective case-control study analyzing chest CT findings in 56 marijuana smokers, 57 nonsmokers, and 33 tobacco-only smokers, marijuana smokers had higher rates of airway changes than did tobacco-only smokers or nonsmokers (P < .001 to P = .04).
■ Emphysema was more common in marijuana smokers than in nonsmokers (75% vs 5%, P < .001) and in age- and sex-matched marijuana smokers than in tobacco-only smokers (93% vs 67%, P = .009); the paraseptal subtype of emphysema was predominant in marijuana smokers.
Marijuana is the most widely used illicit psychoactive substance in the world (1) and the second-most commonly smoked substance after tobacco (2). Its use has increased in Canada since the legalization of nonmedical marijuana in 2018. In 2020, 20% of the population in Canada aged at least 15 years reported having used marijuana in the previous 3 months compared with 14% of the population before marijuana legalization (3). In the United States, the percentage of all adults reporting marijuana use within the previous year rose from 6.7% in 2005 to 12.9% in 2015 (4).
Marijuana is consumed via multiple routes, including smoking, vaporizing, and eating, with inhaled methods being the most common (5). It may be smoked by itself or mixed with tobacco. It is usually smoked without a filter, and users inhale larger volumes with a longer breath hold compared with tobacco smokers (6). For measures of airflow obstruction, one marijuana joint can produce an effect similar to that of 2.5–5.0 tobacco cigarettes (7). Marijuana smoke contains known carcinogens and other chemicals associated with respiratory diseases (8).
Numerous studies have focused on the relationship of marijuana to pulmonary function tests, symptoms, and lung cancer. Two recent systematic reviews (2,9) determined that heavy marijuana use can lead to respiratory symptoms similar to those in tobacco smokers, including cough, sputum production, and wheeze. These are likely related to inflammation of the tracheobronchial mucosa (10) and mucus hypersecretion (11). One study posits that although marijuana causes bronchitis in current users, it does not lead to irreversible airway damage (6). The relationship of marijuana use to pulmonary function test results and lung cancer occurrence is described as equivocal, and both review studies comment on the possibility of the bronchodilatory effect of chronic marijuana smoking leading to a long-term increase in forced vital capacity, a trend also observed in a large population-based cohort study (12). Pulmonary function tests also indicate central airway inflammation in marijuana smokers (6).
To our knowledge, only two previous studies (7,13) have evaluated lung imaging findings in marijuana smokers and neither could establish a clear association between marijuana smoking and emphysema. Other studies investigating this relationship have been case reports and small case series, with little ability to draw clinically relevant conclusions. Other possible lung imaging findings associated with marijuana smoking, such as bronchiectasis, have not been studied.
The purpose of this study was to use chest CT to investigate the effects of marijuana smoking on the lung. We sought to determine if there were identifiable sequelae on chest CT images, including emphysema and signs of airway inflammation.
Materials and Methods
This retrospective case-control study was performed with approval and waiver of informed consent from the local institutional review board. We included chest CT studies obtained prior to November 2020 at The Ottawa Hospital, a tertiary care center, and its affiliate hospitals. Patients were assigned to one of the following three groups: marijuana smokers, nonsmoker control patients, or tobacco-only smokers.
Marijuana smokers.—Cases were identified by searching for the terms marijuana and cannabis in The Ottawa Hospital picture archiving and communications system, and results were filtered to include only those in which chest CT was performed. Charts were reviewed to assess the frequency and duration of marijuana use, as well as for concomitant tobacco use. A total of 56 marijuana smokers were identified with chest CT performed between October 2005 and July 2020. Patient ages were sorted into 5-year age blocks (15–19 years, 20–24 years, 25–30 years, etc), and the number of men and women in each age category was determined. Marijuana consumption was quantified using the conversion of 0.32 g of marijuana per joint, as described by Ridgeway et al (14).
Nonsmoker control patients.—The pool of control patients was identified by searching for the phrase sarcoma initial staging in The Ottawa Hospital picture archiving and communications system. Initial staging chest CT of patients with newly diagnosed sarcoma and without history of smoking, lung disease, or chemotherapy was chosen. Patient charts were reviewed for use of marijuana or tobacco. In the case of marijuana smokers, the patient was excluded from the nonsmoker control group and added to the marijuana smoker group. New control patients were then selected. If the patient smoked only tobacco, he or she was not included in the nonsmoker control group. Fifty-seven control patients were identified with chest CT performed between April 2010 and October 2019. Control subjects were sorted into 5-year age blocks, and an appropriate age- and sex-matched subgroup was created.
Tobacco-only smokers.—The pool of tobacco-only smokers included patients with a chest CT examination performed as part of the high-risk lung cancer screening program (minimum age, 50 years; smoking history, >25 pack-years). Tobacco-only smokers were selected in a similar manner to those in the nonsmoker control group. Patient charts were reviewed for use of marijuana. If marijuana use was identified, the patient was excluded and added to the group of marijuana smokers, and a new patient was selected. Thirty-three tobacco-only smokers were identified with chest CT performed between April and June 2019.
Age- and sex-matched subgroups.—Because the tobacco smoker group included only patients aged at least 50 years, similarly aged patients in the marijuana smoker group and the nonsmoker control group were included in the subgroup analysis.
Chest CT studies were obtained with different multidetector scanners with a section thickness of 2 mm or less. Intravenous iopamidol (Isovue; Bracco Imaging) was used in contrast-enhanced studies. The typical volumetric CT dose index and dose-length product for contrast-enhanced studies were 5.7 mGy and 238.5 mGy · cm, respectively. All images from chest CT studies were reviewed separately by two thoracic fellowship-trained radiologists (G.R., P.S.; 10 and 3 years of experience, respectively), who were blinded to clinical history (ie, marijuana and tobacco use) and other imaging findings. To assess interobserver variability, CT images from 30 patients (10 patients from each group) were reviewed initially. Final statistical analyses were performed on imaging findings obtained using consensus reads involving both radiologists on the entire study population of 146 patients. Lung findings assessed were (a) emphysema and (b) airway changes.
Emphysema.—The predominant pattern of emphysema (paraseptal or centrilobular) was recorded in accordance with Fleischner society descriptions (15).
Airway changes.—Bronchiectasis and bronchial wall thickening (Fig 3A) in accordance with descriptions by Ooi et al (16) and mucoid impaction presence or absence were recorded. The presence or absence of inflammatory small airway disease, in the form of centrilobular nodular opacities (15), also was recorded. Air trapping was not assessed because expiratory acquisitions were not available for all patients.
Non–lung-related findings.—Gynecomastia was recorded with a cutoff dimension of 22 mm of breast tissue (17). Coronary artery calcification was evaluated using the ordinal scoring method previously used by Shemesh et al (18), and a score of 0–12 was recorded for each patient.
Interobserver agreement was evaluated using the Cohen κ statistic. Results were analyzed using χ2 tests to assess for significant differences in rates of emphysema, bronchiectasis, bronchial wall thickening, mucoid impaction, gynecomastia, and coronary artery disease between groups of marijuana smokers, tobacco smokers, and control patients; statistical significance was set at P < .05. Marijuana smokers were compared with control subjects in the main group analysis, and they were compared with both tobacco smokers and control patients in the subgroup analysis. The χ2 tests were performed using an online statistics calculator (https://www.socscistatistics.com/).
A total of 56 marijuana smokers (mean age, 49 years ± 14 [SD]; 34 male, 22 female) and 57 control patients (mean age, 49 years ± 14; 32 male, 25 female) were identified. Patients older than 50 years were included in subgroups for comparison with those who only smoked tobacco; subgroups consisted of 30 marijuana smokers (mean age, 60 years ± 6; 23 male, seven female), 29 control patients (mean age, 61 years ± 6; 17 male, 12 female), and 33 tobacco-only smokers (mean age, 60 years ± 6; 18 male, 15 female). Patient selection criteria are summarized in Figure 1, and patient characteristics are summarized in Table 1.
Our ability to quantify marijuana use was limited, with a daily amount specified in only 28 of 56 patients; average marijuana consumption among these patients was 1.85 g per day (range, 0.25–9.25 g per day). There were 50 of 56 marijuana-smokers who also smoked tobacco, with pack-year data specified in only 47 patients; average smoking history was 25 pack-years (range, 0–100 pack-years) (14).
For tobacco-only smokers, average smoking history was 40 pack-years (range, 25–105 pack-years).
For the analysis of 30 patients, interobserver agreement between the two readers was fair for assessment of bronchiectasis (κ = 0.27), moderate for assessment of bronchial wall thickening (κ = 0.49), substantial for assessment of emphysema (κ = 0.79), and strong for assessment of mucoid impaction (κ = 0.84).
Marijuana Smokers versus Nonsmoker Controls
There were differences in rates of emphysema (both paraseptal and centrilobular) (75% vs 5%, P < .001), bronchial thickening (64% vs 11%, P < .001), bronchiectasis (23% vs 4%, P = .002), and mucoid impaction (46% vs 2%, P < .001) between marijuana smokers and nonsmoker control patients, respectively. No patient had pneumothorax.
Subgroup analysis demonstrated differences in frequency of bronchial thickening (83% vs 21%, P < .001), bronchiectasis (33% vs 7%, P = .012) and mucoid impaction (67% vs 3%, P < .001) between marijuana smokers and nonsmoker control patients, respectively.
Centrilobular nodules were observed in 18% of marijuana smokers while no nonsmoker control patients exhibited this finding (P < .001). Gynecomastia was significantly more common in marijuana smokers than in nonsmoker control patients (38% vs 16%, P = .04). While there was a difference in coronary artery calcification rates between marijuana smokers and nonsmoker control patients (43% vs 26%,), this did not reach statistical significance (P = .06).
Marijuana Smokers versus Tobacco-only Smokers
Differences in bronchial thickening (64% vs 42%, P = .04), bronchiectasis (23% vs 6%, P = .04), and mucoid impaction (46% vs 15%, P = .003) were seen in the non–age-matched marijuana group compared with the tobacco-only group. Subgroup analysis again demonstrated significant differences in rates of bronchial thickening (83% vs 42%, P < .001), bronchiectasis (33% vs 6%, P = .006), and mucoid impaction (67% vs 15%, P < .001) in marijuana smokers compared with tobacco-only smokers. Figure 2 demonstrates CT findings of airway changes in a combined marijuana and tobacco smoker. Variable interobserver agreement limits our ability to draw strong conclusions about bronchial wall thickening and bronchiectasis.
We found no difference between the overall rates of emphysema (including both paraseptal and centrilobular emphysema) when comparing non–age-matched marijuana smokers and tobacco-only smokers (75% vs 67%, P = .40); however, higher rates of emphysema were noted when the age-matched marijuana group was compared with the tobacco-only group (93% vs 67%, P = .01). Also, a significant difference in a paraseptal predominant pattern of emphysema was seen in the marijuana smokers compared with the tobacco-only smokers (57% vs 24%, P = .009) (Fig 3), while we found no evidence of a difference in the proportion of those with a centrilobular pattern (37% vs 39%, P = .82). Rates of the key CT findings in each cohort are summarized for the main group in Table 2 and for the subgroup in Table 3.
In this era of legalization and increasing consumption of marijuana, we sought to identify the imaging features of marijuana smoking on chest CT scans. We found higher rates of emphysema among marijuana smokers (42 of 56, 75%) than among nonsmokers (three of 57, 5%) (P < .001) and among age-matched marijuana smokers (28 of 30, 93%) than among tobacco-only smokers (22 of 33, 67%) (P = .009). Paraseptal emphysema was more predominant in marijuana smokers (27 of 56, 48%) than in tobacco-only smokers (eight of 33, 24%) (P = .03) and in age-matched marijuana smokers (17 of 30, 57%) than in tobacco-only smokers (eight of 33, 24%) (P = .009). Markers of airway inflammation were higher among marijuana smokers than among other groups for both non–age-matched and age-matched subgroup comparisons (P < .001 to P = .04). Gynecomastia was more common in marijuana smokers (13 of 34, 38%) than in control patients (five of 32, 16%) (P = .039) or tobacco-only smokers (two of 18, 11%) (P = .04). There was no evident difference in the presence of coronary artery calcification between age-matched marijuana smokers (21 of 30, 70%) and tobacco-only smokers (28 of 33, 85%) (P = .16).
It has been posited that certain maneuvers performed by marijuana smokers, such as full inhalation with a sustained Valsalva maneuver, may lead to microbarotrauma and peripheral airspace changes, such as apical bullae. In our study, paraseptal emphysema was the predominant pattern seen in marijuana smokers, while centrilobular emphysema was the predominant pattern seen in tobacco-only smokers. This may represent an earlier stage of apical bulla formation reported in marijuana smokers (19,20) and may explain the absence of the typical pulmonary function test changes of chronic obstructive pulmonary disease in marijuana smokers. The χ2 tests revealed similar overall rates of emphysema in the non–age-matched marijuana smoker group and the tobacco-only smoker groups and higher rates of emphysema among age-matched marijuana smokers compared with tobacco-only smokers. This is in contradistinction to a study by Ruppert et al (21), which showed similar prevalence of emphysema among 38 tobacco-only smokers and 32 tobacco and marijuana smokers but occurrence of emphysema in the latter group at a younger age. We were not able to establish a definite association between marijuana smoking and emphysema or bullous disease. Causality needs to be further examined in larger patient cohorts with prospective accurate quantification data, given the increasing body of evidence suggesting an association between smoking marijuana and spontaneous pneumothorax (22,23).
Bronchiectasis, bronchial wall thickening, and mucoid impaction are CT indicators of airway inflammation. Our findings suggest that smoking marijuana leads to chronic bronchitis in addition to the airway changes associated with smoking tobacco. This is especially striking given the extensive smoking history of patients in the tobacco-only group (smoking history, 25–100 pack-years). In addition, our results were still significant when comparing the non–age-matched groups, including younger patients who smoked marijuana and who presumably had less lifetime exposure to cigarette smoke. Further studies in larger cohorts are needed to better define imaging correlates of airway inflammation and chronic bronchitis that have been described in association with marijuana smoking in previous clinical studies and systematic literature reviews (2,24).
Poorly defined centrilobular ground-glass nodules can denote inflammatory small airway disease corresponding to the entity of respiratory bronchiolitis characterized by accumulation of pigmented histiocytes adjacent to respiratory bronchioles and alveolar ducts and sacs. This finding is commonly related to cigarette smoking (25,26) but can be related to inhalation of a variety of toxic particles (15). A histopathologic study comparing 10 marijuana smokers with five tobacco smokers and five nonsmokers reported that marijuana smoking was associated with massive intra-alveolar accumulation of pigmented histiocytes evenly throughout the pulmonary parenchyma, assumed to be related to higher particulate matter concentration and deeper and longer inhalation techniques used by marijuana smokers (27). In our study, we found no differences in the occurrence of centrilobular nodules between marijuana smokers and tobacco-only smokers. However, this may be because 89% (50 of 56) marijuana smokers were also tobacco smokers. Further assessment in imaging-based studies with larger patient cohorts and better quantification data are required. Furthermore, biopsy confirmation may be needed to better understand the histopathology of these nodules in marijuana smokers: Are they related to respiratory bronchiolitis or organizing pneumonia (described by Berkowitz et al ).
We were unable to confirm an association between coronary artery calcification and marijuana smoking, similar to a systematic review of 24 articles that reported that evidence on the association of marijuana use with cardiovascular risk factors is insufficient to make conclusions (29). At least one recent study of 146 young marijuana users with chest pain found that marijuana use did not confer additional risk of coronary artery disease, as detected with coronary CT angiography (30). Tobacco smoking, on the other hand, is an established risk factor for coronary artery disease (31). Our study also enabled us to confirm the well-known relationship between regular long-term marijuana use and gynecomastia (32).
Our study had limitations. First, the small sample size precluded us from drawing strong conclusions. Second, the retrospective nature of the study had its own inherent limitations. Third, there was inconsistent quantification of patient marijuana use, due in part to the previous illegal nature of marijuana possession, which led to a lack of patient reporting. Accurate quantification is further complicated by the fact that users often share joints, use different inhalation techniques, and use marijuana of varying potency. Fourth, given that most marijuana smokers also smoke tobacco, the synergistic effects of these two substances cannot be effectively evaluated. Fifth, only a portion of patients could be age matched, since the tobacco-only cohort was taken from the lung cancer screening study and the patients were aged at least 50 years. Due to the age mismatch in the larger cohort, there are differences in the duration of smoking. Lastly, variable interobserver agreement limits our ability to draw strong conclusions about bronchial wall thickening and bronchiectasis.
In conclusion, our study suggests that distinct radiologic findings in the lung may be seen in marijuana smokers, including higher rates of paraseptal emphysema and airway inflammatory changes, such as bronchiectasis, bronchial wall thickening, and mucoid impaction when compared with nonsmoker control patients and those who only smoke tobacco. These findings may be related to specific inhalational techniques while smoking marijuana, as well as to the bronchodilatory and immunomodulatory properties of its components. Further larger and prospective studies are necessary to confirm and further elucidate these findings, as marijuana use is bound to increase in the future, given the increasing legalization of its use for medical and recreational purposes.
Disclosures of conflicts of interest: L.M. No relevant relationships. P.S. No relevant relationships. J.P.S. No relevant relationships. M.D.F.M. Radiology editorial board. G.R. Legal advice for BLG firm.
Author contributions: Guarantors of integrity of entire study, L.M., P.S., G.R.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; approval of final version of submitted manuscript, all authors; agrees to ensure any questions related to the work are appropriately resolved, all authors; literature research, L.M., P.S., M.D.F.M., G.R.; clinical studies, G.R.; statistical analysis, L.M., J.P.S., M.D.F.M., G.R.; and manuscript editing, all authors
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Governments seek buyer as Quebec COVID-19 vaccine manufacturer Medicago set to close
Quebec Economy Minister Pierre Fitzgibbon said Friday the province has had preliminary talks with potential buyers in the pharmaceutical sector to keep Medicago’s expertise and skilled workforce in Quebec. He said both the Quebec and federal governments would be willing to put in money to secure a deal.
“We can’t operate it ourselves; the government will not be the main shareholder,” Fitzgibbon said. “But if there is a pharmaceutical company that considers it’s worth continuing, we’re ready to help.”
Mitsubishi Chemical said Thursday it would stop marketing the Medicago-produced Covifenz vaccine, which is plant-based and was approved by Health Canada one year ago for adults aged 18 to 64.
The Japanese chemical company said it had been preparing to commercially produce the Covifenz vaccine but decided against doing so because of the “significant changes” in the COVID-19 vaccine environment. The company said it would dissolve Medicago because it is no longer “viable” to continue marketing its products.
“In light of significant changes to the COVID-19 vaccine landscape since the approval of Covifenz, and after a comprehensive review of the current global demand and market environment for COVID-19 vaccines and Medicago’s challenges in transitioning to commercial-scale production, the (company) has determined that it will not pursue the commercialization of Covifenz,” Mitsubishi Chemical said in a statement.
Following the announcement, Medicago issued a statement thanking its employees. “The Medicago team has pushed scientific boundaries and we know that they will continue to make incredible contributions to innovation and biopharmaceutical’s sector.”
Canada invested $173 million in Medicago in 2020 to support development of the Covifenz vaccine and help Medicago expand its production facility in Quebec City.
On Thursday, Innovation, Science and Industry Minister François-Philippe Champagne told reporters the federal government is in “solution mode.”
“Our first order of business is really to try to find a partner who can help us preserve the jobs, preserve the technology and the intellectual property,” Champagne said.
The minister acknowledged that mRNA vaccine technology for COVID-19 became dominant as it “seemed to be most effective.”
But Medicago’s plant-based vaccine was still “promising,” Champagne said.
“Everyone agreed that the plant-based vaccine could very well help in a future pandemic,” Champagne said.
Speaking to reporters on Montreal’s South Shore Friday, Fitzgibbon said the company informed the province at the end of December it intended to pull the plug on Medicago.
In May 2015, Quebec and Ottawa announced loans of $60 million and $8 million, respectively, for the construction of a complex in the Quebec City region to house Medicago’s activities.
“The challenge is not (getting the loan repaid), it’s how we can save the jobs, save this company,” Fitzgibbon said.
While Canada authorized Medicago’s vaccine in February 2022, it was rejected for emergency use by the World Health Organization in March because tobacco company Philip Morris was a minority shareholder in the company, contravening a policy adopted in 2005 by the United Nations agency.
Quebec City Mayor Bruno Marchand said on Twitter he was saddened by the closure of the company.
“My thoughts are with the families who learned some very sad news,” Marchand said Thursday evening. “We have to roll up our sleeves to keep all this expertise in the field of health innovation in Quebec City.”
This report by The Canadian Press was first published Feb. 3, 2023.
Sidhartha Banerjee, The Canadian Press
Bird flu keeps spreading beyond birds. Scientists worry it signals a growing threat to humans, too
As a deadly form of avian influenza continues ravaging bird populations around much of the world, scientists are tracking infections among other animals — including various types of mammals more closely related to humans.
Throughout the last year, Canadian and U.S. officials detected highly pathogenic H5N1 avian flu in a range of species, from bears to foxes. In January, France’s national reference laboratory announced that a cat suffered severe neurological symptoms from an infection in late 2022, with the virus showing genetic characteristics of adaptation to mammals.
Most concerning, multiple researchers said, was a large, recent outbreak on a Spanish mink farm.
Last October, farm workers began noticing a spike in deaths among the animals, with sick minks experiencing an array of dire symptoms like loss of appetite, excessive saliva, bloody snouts, tremors, and a lack of muscle control.
The culprit wound up being H5N1, marking the first known instance of this kind of avian influenza infection among farmed minks in Europe, notes a study published in Eurosurveillance this month.
“Our findings also indicate that an onward transmission of the virus to other minks may have taken place in the affected farm,” the researchers wrote.
Eventually, the entire population of minks was either killed or culled — more than 50,000 animals in total.
That’s a major shift, after only sporadic cases among humans and other mammals over the last decade, according to Michelle Wille, a researcher at the University of Sydney who focuses on the dynamics of wild bird viruses.
“This outbreak signals the very real potential for the emergence of mammal-to-mammal transmission,” she said in email correspondence with CBC News.
It’s only one farm, and notably, none of the workers — who all wore face shields, masks, and disposable overalls — got infected.
But the concern now, said Toronto-based infectious disease specialist Dr. Isaac Bogoch, is if this virus mutates in a way that allows it to become increasingly transmissible between mammals, including humans, “it could have deadly consequences.”
“This is an infection that has epidemic and pandemic potential,” he said. “I don’t know if people recognize how big a deal this is.”
H5N1 has high mortality rate
Among birds, the mortality rate of this strain of highly pathogenic avian influenza can be close to 100 per cent, causing devastation to both wild bird populations and poultry farms.
It’s also often deadly for other mammals, humans included.
The World Health Organization (WHO) has documented 240 cases of H5N1 avian influenza within four Western Pacific countries — including China, Cambodia, Laos, and Vietnam — over the last two decades. More than half of the infected individuals died.
Global WHO figures show more than 870 human cases were reported from 2003 to 2022, along with at least 450 deaths — a fatality rate of more than 50 per cent.
Bogoch said the reported death toll may be an overestimate, since not all infections may be detected, though it’s clear people can “get very, very sick from these infections.”
Most human infections also appeared to involve people having direct contact with infected birds. Real-world mink-to-mink transmission now firmly suggests H5N1 is now “poised to emerge in mammals,” Wille said — and while the outbreak in Spain may be the first reported instance of mammalian spread, it may not be the last.
“A virus which has evolved on a mink farm and subsequently infects farm workers exposed to infected animals is a highly plausible route for the emergence of a virus capable of human-to-human transmission to emerge,” she warned.
Louise Moncla, an assistant professor of pathobiology at the University of Pennsylvania school of veterinary medicine, explained that having an “intermediary host” is a common mechanism through which viruses adapt to new host species.
“And so what’s concerning about this is that this is exactly the kind of scenario you would expect to see that could lead to this type of adaptation, that could allow these viruses to replicate better in other mammals — like us.”
Surveillance, vaccines both needed
What’s more reassuring is the ongoing development of influenza vaccines, giving humanity a head start on the well-known threat posed by bird flu.
Wille noted the earlier spread of H7N9, another avian influenza strain which caused hundreds of human cases in the early 2010s, prompted similar concern that the virus would acquire the mutations needed for ongoing human-to-human transmission.
“However, a very aggressive and successful poultry vaccination campaign ultimately stopped all human cases,” she added.
But while several H5N1 avian influenza vaccines have been produced, including one manufactured in Canada, there’s no option approved for public use in this country.
To ward off the potential threat this strain poses to human health, Bogoch said ongoing surveillance and vaccine production needs to remain top-of-mind for both policy makers and vaccine manufacturers.
Dr. Jan Hajek, an infectious diseases physician at Vancouver General Hospital, also questioned whether it’s time to wind down global mink farming, given the spread of various viruses, from avian influenza to SARS-CoV-2, the virus behind COVID-19.
“We’re closely related to minks and ferrets, in terms of influenza risks … if it’s propagating to minks, and killing minks, it’s worrisome to us,” he said.
In 2021, B.C. officials announced an end to mink farming across the province, saying the farms can be reservoirs for viruses and represent an ongoing danger to public health. All mink farm operations must be shut down, with all of the pelts sold, by April 2025.
However, other provinces — and plenty of countries — do intend to keep their mink farms operating.
“Is it responsible to have these kinds of farming conditions where these types of events can occur?” questioned Moncla. “If we’re going to keep having these types of farms, what can we do to make this safer?”
6,654 students facing suspension due to out-of-date immunization records
The Windsor-Essex County Health Unit (WECHU) has issued about 6,654 suspension orders to students who do not meet immunization requirements.
WECHU completed a review of all elementary student immunization records in December and more than 12,000 students received a notice.
These students were either overdue for one or more vaccines required to attend school, or their immunization records were not updated with the health unit.
“While many of these vaccines are normally administered by primary health care providers, parents and guardians of children who received their vaccines from their health care provider still need to report this information to the health unit,” said a WECHU news release.
The Immunization of School Pupils Act (ISPA) (1990), Section 11, Subsections (1) and (2) requires public health units to maintain and review vaccine records for every student attending school and to enforce a school suspension for incomplete immunization information. As the next step of the ISPA enforcement process, orders were mailed out to students that do not meet this requirement.
WECHU said this is the final notice.
The suspension order notifies parents and guardians that immunization records must be updated to the WECHU by Thursday, March 16, at 6 p.m. or their child will be suspended for up to 20 days from school, starting Monday, March 20, 2023. Once parents and guardians provide the missing immunization information to the WECHU, the student is removed from the suspension list and can attend school again.
Under the ISPA , children can be exempted from immunization for medical reasons or due to conscience or religious belief.
Families can book immunization appointments with their health care provider and are reminded to update their child’s immunization records online at immune.wechu.org.
Catch-up immunization clinics are also being offered at the WECHU Windsor and Leamington offices and will continue until the end of March. Families can book an appointment at a WECHU clinic by visiting wechu.org/getimmunized or by calling the WECHU at 519-960-0231.
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