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VICTORIA — British Columbia Premier David Eby said the temporary foreign worker program should "be cancelled or significantly reformed" because the province can't have an immigration system that's linked to high youth unemployment, while putting pressure on homeless shelters and food banks.
Eby said Thursday that one reason the province is facing "significant fiscal headwinds" is because of "very high unemployment rates" among young people, which he linked to both the temporary foreign worker program and the international student program.
"We can't have an immigration system that outpaces our ability to build schools, and housing, and we can't have an immigration program that results in high unemployment," Eby said Thursday after making an unrelated announcement at a school in Surrey, B.C.
His remarks came a day after similar comments from Conservative Leader Pierre Poilievre, who blamed the program for an employment crisis among young Canadians and called for it to be scrapped.
The premier said B.C. was willing to "convene provinces that are interested in this issue" to have a "serious, grown-up" conversation about immigration in Canada and its impact on critical infrastructure, such as housing and schools.
Employment and Social Development Canada says the temporary foreign worker program allows Canadian employers to hire foreign workers to fill temporary jobs when qualified Canadians are not available.
The Canadian Federation of Independent Businesses said the calls to scrap the program are "deeply misguided," and instead of putting Canadians in jobs, they could put the jobs of Canadians at risk.
Ryan Mitton, the federation's director of legislative affairs for B.C., said in a statement that the temporary foreign worker program was the "last resort that keeps the doors open" for many small businesses in the province, especially in rural and remote areas.
"Without the program, many B.C. restaurants, farms and care providers would shut down, which would displace Canadian workers as well," Mitton said.
He said adjustments to the program could be made, "but cancelling it altogether puts politics ahead of sensible policy."
B.C.'s youth unemployment rate for people aged 15 to 24 was 12.1 per cent in July, below the Canadian rate of 14.6 per cent, Statistics Canada figures show.
A 2024 report by Food Banks BC, which represents more than 100 food relief organizations in the province, found a "significant increase" in the number of immigrant or refugee clients to the food banks, as well as women and those in racialized communities.
The report said 26 per cent of food bank users identified as immigrants or refugees with the figure rising to 39 per cent in the Vancouver coastal region. The report did not identify whether users were temporary foreign workers.
Poilievre said Wednesday that cancellation of the temporary foreign worker program should include exceptions for difficult-to-fill agricultural jobs, while Eby said the government must address the "concerns of farmers and others" that "legitimately" need temporary labour.
He called it a "very timely issue" for the federal government to consider.
Prime Minister Mark Carney said Wednesday that his government would review the program but also added that it "has a role to play."
Eby said Carney's government has taken "some good steps to rein in the excesses" of the program but Ottawa needs to do more.
Statistics Canada says there were 356,000 temporary foreign workers in Canada in 2011, rising to 845,000 in 2021.
Canada set a target to admit 82,000 new temporary foreign workers this year.
Conservative Party of BC Leader John Rustad said sectors like agriculture and tourist destinations like Whistler are in "desperate need" of temporary foreign workers. "However, it is clear in my mind that the immigration system is broken, and has been broken for a number of years by Ottawa," he said.
British Columbia, like Quebec, should take control of immigration to develop a "made-in-BC solution," he added.
This report by The Canadian Press was first published on Sept. 4, 2025.
Wolfgang Depner, The Canadian Press
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The United States and Europe have long used unilateral sanctions as a tool of imperial power, to discipline and even destroy Global South governments that seek to shake off Western domination, chart an independent path, and establish any kind of meaningful sovereignty.
During the 1970s, there were, on average, about 15 countries under Western unilateral sanctions in any given year. In many cases, these sanctions sought to strangle access to finance and international trade, destabilise industries, and inflame crises to provoke state collapse.
For instance, when the popular socialist Salvador Allende was elected to power in Chile in 1970, the US government imposed brutal sanctions on the country. At a September 1970 meeting at the White House, US President Richard Nixon explained the objective was to “make [Chile’s] economy scream”. The historian Peter Kornbluh describes the sanctions as an “invisible blockade” that cut Chile off from international finance, created social unrest, and paved the way for the US-backed coup that installed the brutal right-wing dictatorship of Augusto Pinochet.
Since then, the US and Europe have dramatically increased their use of sanctions. During the 1990s and 2000s, an average of 30 countries were under Western unilateral sanctions in any given year. And now, as of the 2020s, it is more than 60 – a strikingly high proportion of the countries of the Global South.
Sanctions often have a huge human toll. Scholars have demonstrated this in several well-known cases, such as the US sanctions against Iraq in the 1990s that led to widespread malnutrition, lack of clean water, and shortages of medicine and electricity. More recently, US economic warfare against Venezuela has resulted in a severe economic crisis, with one study estimating that sanctions caused 40,000 excess deaths in just one year, from 2017 to 2018.
Until now, researchers have sought to understand the human toll of sanctions on a case-by-case basis. This is difficult work and can only ever give us a partial picture. But that has changed with new research published this year in The Lancet Global Health, which gives us a global view for the first time. Led by the economist Francisco Rodriguez at the University of Denver, the study calculates the total number of excess deaths associated with international sanctions from 1970 to 2021.
The results are staggering. In their central estimate, the authors find that unilateral sanctions imposed by the US and EU since 1970 are associated with 38 million deaths. In some years, during the 1990s, more than a million people were killed. In 2021, the most recent year of data, sanctions caused more than 800,000 deaths.
According to these results, several times more people are killed by sanctions each year than are killed as direct casualties of war (on average, about 100,000 people per year). More than half of the victims are children and the elderly, people who are most vulnerable to malnutrition. The study finds that, since 2012 alone, sanctions have killed more than one million children.
Hunger and deprivation are not an accidental by-product of Western sanctions; they are a key objective. This is clear from a State Department memo written in April 1960, which explains the purpose of US sanctions against Cuba. The memo noted that Fidel Castro – and the revolution more broadly – enjoyed widespread popularity in Cuba. It argued that “every possible means should be undertaken promptly to weaken the economic life of Cuba,” by “denying money and supplies to Cuba, to decrease monetary and real wages, to bring about hunger, desperation and overthrow of government”.
The power of Western sanctions hinges on their control over the world’s reserve currencies (the US dollar and the Euro), their control over international payment systems (SWIFT), and their monopoly over essential technologies (eg satellites, cloud computation, software). If countries in the Global South wish to chart a more independent path towards a multipolar world, they will need to take steps to limit their dependence in these respects and thus insulate themselves from backlash. The recent experience of Russia shows that such an approach can succeed.
Governments can achieve greater independence by building South-South trade and swap lines outside the core currencies, using regional planning to develop necessary technologies, and establishing new payment systems outside Western control. Indeed, several countries are already taking steps in this direction. Importantly, new systems that have been developed in China (eg CIPS for international payments, BeiDou for satellites, Huawei for telecom) now provide other global South countries alternative options that can become a pathway out of Western dependence and the sanctions net.
These steps are necessary for countries that wish to achieve sovereign development, but they are also a moral imperative. We cannot accept a world where half a million people are killed each year to prop up Western hegemony. An international order that relies on this kind of violence must be dismantled and replaced.
The views expressed in this article are the author’s own and do not necessarily reflect Al Jazeera’s editorial stance.
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Around 5–10% of people with COVID infections go on to experience long COVID, with symptoms lasting three months or more.
Researchers have proposed several biological mechanisms to explain long COVID. However, in a perspective article published in the latest Medical Journal of Australia, we argue that much, if not all, long COVID appears to be driven by the virus itself persisting in the body.
Since relatively early in the pandemic, there has been a recognition that in some people, SARS-CoV-2 – or at least remnants of the virus – could stay in various tissues and organs for extended periods. This theory is known as “viral persistence”.
While the long-term presence of residual viral fragments in some people’s bodies is now well established, what remains less certain is whether live virus itself, not just old bits of virus, is lingering – and if so, whether this is what causes long COVID. This distinction is crucial because live virus can be targeted by specific antiviral approaches in ways that “dead” viral fragments cannot.
Viral persistence has two significant implications:
when it occurs in some highly immunocompromised people, it is thought to be the source of new and substantially different-looking variants, such as JN.1
it has the potential to continue to cause symptoms in many people in the wider population long beyond the acute illness. In other words, long COVID could be caused by a long infection.
What does the research say?
While there remains no single study that confirms that persistent virus is the cause of long COVID, collectively several recent key papers make a compelling case.
In February, a study in Nature found a high number of people with mild COVID symptoms had extended periods of shedding the genetic material of the virus, so-called viral RNA, from their respiratory tract. Those with persistent shedding of this viral RNA – which almost certainly represents the presence of live virus – were at higher risk of long COVID.
Other key papers detected replicating viral RNA and proteins in blood fluid of patients years after their initial infection, a sign that the virus is likely replicating for long periods in some hidden reservoirs in the body, perhaps including blood cells.
Another study detected viral RNA in ten different tissue sites and blood samples 1–4 months after acute infection. This study found the risk of long COVID (measured four months following infection) was higher in those with persistently positive viral RNA.
The same study also gave clues about where in the body the persisting virus resides. The gastrointestinal tract is one site of considerable interest as a long-term viral hideout.
Earlier this week, further evidence of persistent virus increasing likelihood of long COVID has been published as part of the RECOVER initiative, a collaborative research project that aims to address the impacts of long COVID.
However, formal proof that virus capable of replicating can last for years in the body remains elusive. This is because isolating the live virus from reservoirs inside the body where the virus “hides” is technically challenging.
In its absence, we and other scientists argue the cumulative evidence is now sufficiently compelling to galvanise action.
What needs to happen next?
The obvious response to this is to fast-track trials of known antivirals for prevention and cure of long COVID.
This should include more left-field therapies such as the diabetes drug metformin. This has possible dual benefits in the context of long COVID:
its antiviral properties, which have demonstrated surprising efficacy against long COVID
as a potential therapeutic in treating impairments related to fatigue.
However, another major thrust should be the development of new drugs and the establishment of clinical trial platforms for rapid testing.
Science has uncovered exciting therapeutic options. But translating these into forms usable in the clinic is a large hurdle that requires support and investment from governments.
Demystify and preventing long COVID
The notion of “long infection” as a contributor or even the driver of long COVID is a powerful message. It could help demystify the condition in the eyes of the wider community and increase awareness among the general public as well as medical professionals.
It should help raise awareness in the community of the importance of reducing rates of re-infection. It is not just your first infection, but each subsequent COVID infection carries a risk of long COVID.
Long COVID is common and isn’t restricted to those at high risk of severe acute disease but affects all age groups. In one study, the highest impact was in those aged 30 to 49 years.
So, for now, we all need to reduce our exposure to the virus with the tools available, a combination of:
clean indoor air approaches. In its simplest form, this means being conscious of the importance of well-ventilated indoor spaces, opening the windows and improving airflow as COVID spreads through air. More sophisticated ways of ensuring indoor air is safe involve monitoring quality and filtering air in spaces that cannot be easily naturally ventilated
using high-quality masks (that are well-fitting and don’t let air in easily, such as N95-type masks) in settings where you don’t have confidence of the quality of the indoor air and/or that are crowded
testing, so you know when you’re positive. Then, if you’re eligible, you can get treatment. And you can be vigilant about protecting those around you with masks, staying at home where possible, and ventilating spaces
staying up to date with COVID booster doses. Vaccines reduce long COVID and other post-COVID complications.
Hopefully one day there will be better treatments and even a cure for long COVID. But in the meantime, increased awareness of the biomedical basis of long COVID should prompt clinicians to take patients more seriously as they attempt to access the treatments and services that already exist.
Read more: The latest COVID booster will soon be available. Should I get one? Am I eligible?
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ReseaRch aRticles
Science 26 June 2025 1422
aDaPtatiON
Rapid polygenic adaptation
in a wild population of ash trees
under a novel fungal epidemic
Carey L. Metheringham1,2 †, William J. Plumb1,2,3
‡,
William R. M. Flynn4,5
, Jonathan J. Stocks1,2 §, Laura J. Kelly 1,2 ,
Miguel Nemesio Gorriz3
¶, Stuart W. D. Grieve4,6
, Justin Moat2
,
Emily R. Lines7
, Richard J. A. Buggs1,2 *, Richard A. Nichols1
*
Rapid evolution through small shifts in allele frequencies at
thousands of loci is a long-standing neo-Darwinian prediction but
is hard to characterize in the wild. european ash tree (Fraxinus
excelsior) populations have recently come under strong selection
by the invasive fungal pathogen Hymenoscyphus fraxineus. using
genomic prediction models based on field trial phenotypes and
7985 loci, we show a shift in genomically estimated breeding
values in an ancient woodland, between adult trees established
before the epidemic started and juvenile trees established since.
using simulations, we estimate that natural selection has
eliminated 31% of the juvenile population. Thus, we document a
highly polygenic heritable microevolutionary adaptive change
over a single generation in the wild.
Whether complex traits typically adapt to new environments through
large allele frequency changes in a few loci or through small allele fre-
quency changes in many loci is an open question in evolutionary biology
(1–5). While theory suggests that a highly polygenic response should be
rapid and effective (3–6), it is far easier in nature for population geneti-
cists to demonstrate cases of natural selection involving low numbers
of loci with a large effect size (7–10). Although the methods of quantita-
tive genetics can show, by statistical comparison of related individuals,
that additive genetic variance exists for complex traits under selection,
it has often not been possible to show by these methods that response
to selection is occurring (11–14). This situation has led to a disconnect
between population genetics and quantitative genetics. Genomic predic-
tion approaches, developed for agricultural breeding, that use genome-
wide single-nucleotide polymorphism (SNP) data to predict individuals’
genetic merit for a quantitative trait of interest, can enable us to bridge
this gap (5, 15, 16). If we can show genome-wide allele frequency differ-
ences before and after the arrival of a new selective pressure (17) or in
different age classes at a single time point (12, 18–22), affecting genetic
merit, a polygenic response to selection could be demonstrated.
The possibility of a rapid adaptive response is of particular interest
in the case of the ash dieback epidemic that has swept across Europe
in the past three decades, caused by the fungus Hymenoscyphus
fraxineus, an invasive from East Asia (23). Numerous studies based
on planted trials suggest that heritable variation in susceptibility to
the fungus exists within European ash (Fraxinus excelsior) populations
(24–27). The intensity of selection on viability may be stronger in
smaller, younger ash trees, as they are observed to die more rapidly
from ash dieback infection than larger, older trees (28, 29). Rapid
juvenile mortality may occur because the fungus can more quickly
encircle the main stem and because smaller trees are closer to the
leaf litter where H. fraxineus apothecia are produced. Recruitment
of the next generation may also be affected by reduced reproduction
by adult trees damaged but not yet killed by the fungus (30, 31).
It has been hypothesized that mortality of susceptible juvenile trees
and reduced reproduction by susceptible adult trees will drive changes in
allele frequencies leading to an increase in disease resistance in the next
generation of ash (24, 27). In a previous study, based on 38,784 ~7-year-old
ash trees from British, Irish, and German provenances growing in field
trials, we sequenced the 623 healthiest trees [a score of 7 on the scale of
Pliūra et al. (32)] and 627 trees whose woody tissues were highly damaged
by ash dieback (mainly scores 4 or 5). We used a genome-wide association
study (GWAS) to rank loci associated with these phenotypes by P value
(26) and used sets from 100 to 50,000 of the top loci to train genomic
prediction models, which were tested on 148 trees. We found that 10,000
loci gave genomic estimated breeding values (GEBVs) with the highest
frequency of correct allocations of test trees (0.67) (26). We here calculate
that these GEBVs explained 24.0% [confidence interval (CI): 11.5 to 37.0%]
of the phenotypic variation in the test population’s damage due to the
fungus (see materials and methods in the supplementary materials).
If natural selection is acting on natural ash populations under high
disease pressure, we would expect to see GEBVs increase in the
younger generation of trees that have been exposed to infection since
germination, with shifts in allele frequencies that correlate with their
effect sizes. In this study, we tested this hypothesis in a woodland lo-
cated within the geographic sample range of Stocks et al. (26).
Phenotypic and genomic characterization of an ash population
Our study site, Marden Park wood, is an ancient seminatural woodland
dominated by F. excelsior, where the pathogen H. fraxineus is thought
to have been present since 2012 (fig. S1). It is located in UK Native
Seed Zone number 405, a provenance included in the previous trials
(26). Phenotypic assessments of this woodland in 2019, when we col-
lected ash tissue samples for sequencing, found H. fraxineus symptoms
on the majority of trees (Fig. 1) and no evidence for felling or removal
of dead trees. Damage from the fungus had further increased by 2021,
especially in juvenile trees (Fig. 1). This fits with widespread documen-
tation of the ongoing progress of the ash dieback epidemic throughout
Europe (29, 33).
We generated short-read sequence data for 580 individuals (128
adults, which had established pre-epidemic, and 452 post-epidemic
juveniles; fig. S2) and 30 technical replicates at ∼11× whole-genome
coverage and estimated allele frequencies at ~9 million SNP loci. Of the
10,000 SNPs used for genomic prediction in the trials (see above), 7985
were variable in the Marden Park dataset and passed allele frequency
and quality thresholds. This smaller number of polymorphic SNPs re-
flects the lower genetic diversity present in Marden Park wood than in
the planted trials, which included many seed zones. Of the 2015 SNPs
that were not variable in the Marden Park population, 1055 were fixed
for the allele associated with low ash dieback damage in the planted
trials and 960 for the allele associated with high damage.
We calculated GEBVs for the Marden Park trees from the 7985 poly-
morphic SNPs using the parameters of the genomic prediction model
trained on the field trials (26). Our visual assessments of ash dieback
damage, scored on a five-point scale for juveniles (a similar method to
that used in the trials) and as percentage canopy cover in adults,
showed no significant relationship with individual’s GEBV scores
(figs. S3 and S4). A weak relationship between individual GEBVs and
phenotypes assessed in the field is expected because of the large envi-
ronmental component of damage phenotypes in the wild, owing to local
microenvironments, age differences within cohorts, and presence of
other microorganisms. In addition, the phenotypic scoring method we
1
School of Biological and Behavioural Sciences, Queen Mary University of London, London, UK.
2
Science Directorate, Royal Botanic Gardens, Kew, Richmond upon Thames, UK. 3
Forestry
Development Department, Teagasc, Dublin, Republic of Ireland. 4
School of Geography, Queen
Mary University of London, London, UK. 5
Department of Plant Sciences, University of Cambridge,
Cambridge, UK. 6
Digital Environment Research Institute, Queen Mary University of London,
London, UK. 7
Department of Geography, University of Cambridge, Cambridge, UK. *Corresponding
author. Email: r.buggs@kew.org (R.J.A.B.); r.a.nichols@qmul.ac.uk (R.A.N.) †Present address:
School of Life Sciences, University of Dundee, Nethergate, Dundee, Scotland, UK. ‡Present
address: Jealott’s Hill International Research Centre, Syngenta, Bracknell, Berkshire, UK.
§Present address: Forestry England, Lyndhurst, Hants, UK. ¶Present address: Mejora y
Conservación de Recursos Genéticos Forestales, Grupo Tragsa–SEPI, Paterna, Valencia, Spain.CORRECTED 23 JULY 2025; SEE LAST PAGEDownloaded from <a href="https://www.science.org" rel="nofollow">https://www.science.org</a> at University of British Columbia on September 03, 2025
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