Long-term exposure to common air pollutants may significantly raise the risk of developing substance use disorders, while living surrounded by greenery appears to offer a measure of protection, according to a large new population-based study drawing on nearly a quarter of a million participants from the UK Biobank.

The research, published in BMC Psychiatry, analyzed data from 247,138 UK Biobank participants who were free of substance use disorders at baseline, tracking them over a median follow-up period of 10.9 years. During that time, 4,982 participants went on to develop a substance use disorder, providing the researchers with a robust dataset to examine the relationship between environmental exposures and mental health outcomes.

The study, led by Huan Liu and Bolun Cheng of Xi’an Jiaotong University in China, along with colleagues including Feng Zhang, represents one of the most comprehensive investigations to date into how the air people breathe and the greenness of their neighborhoods may influence vulnerability to addiction. The findings arrive at a moment when urban planners and public health officials are increasingly recognizing that the built and natural environments shape health in ways that extend well beyond respiratory and cardiovascular disease.

To assess air pollution exposure, the team employed Land Use Regression modeling to estimate concentrations of five pollutants at each participant’s residential address: fine particulate matter known as PM2.5, coarse particulate matter classified as PM2.5−10, the larger particulate fraction PM10, nitrogen dioxide (NO2), and nitrogen oxides (NOX). These pollutants, produced primarily by traffic, industry, and combustion sources, have long been associated with a range of physical health problems, but their role in psychiatric and behavioral conditions has remained far less certain.

For residential greenness, the researchers turned to the 2005–2007 Land Cover Map, measuring three distinct aspects of the environment within a 300-meter buffer around each home: the proportion of green space, the presence of a domestic garden, and the extent of natural environment. This tripartite approach allowed the investigators to distinguish between different types of vegetation and their potentially different effects on health.

Using Cox proportional hazards models, the team calculated hazard ratios with 95 percent confidence intervals to quantify the association between each exposure and the risk of developing a substance use disorder. The results were striking in their consistency. All five air pollutants were positively associated with incident SUD in fully adjusted models that controlled for a wide range of potential confounders.

Fine particulate matter, or PM2.5, showed the strongest effect, with a hazard ratio of 1.111 (95 percent CI: 1.081–1.142), followed by PM10 with a hazard ratio of 1.070 (95 percent CI: 1.054–1.086). These figures indicate that higher exposure to particulate pollution was associated with a measurable increase in the likelihood of developing a substance use disorder over the follow-up period, even after accounting for demographic, socioeconomic, and behavioral factors.

On the protective side of the ledger, two of the three greenness measures emerged as significant. Green space was inversely associated with SUD risk, showing a hazard ratio of 0.997 (95 percent CI: 0.996–0.998), and the natural environment measure produced an identical finding, with a hazard ratio of 0.997 (95 percent CI: 0.995–0.998). While these effect sizes appear modest on a per-unit basis, they represent population-level signals across a very large cohort, suggesting that even incremental increases in neighborhood greenness may contribute to reduced vulnerability.

Perhaps the most intriguing finding of the study concerns the interaction between pollution and greenery. The researchers tested whether residential greenness modified the association between air pollutants and SUD risk by introducing cross-product terms into their models and evaluating them with likelihood-ratio tests. The results pointed to a buffering role for domestic gardens specifically. Among participants in the high-exposure subgroup, the presence of a domestic garden attenuated the positive associations between pollutants and SUD, with cross-product terms of 0.979 (95 percent CI: 0.963–0.996) for PM2.5 and 0.987 (95 percent CI: 0.980–0.995) for PM10.

In practical terms, this suggests that having access to a private garden may partially offset some of the harm associated with living in areas of elevated particulate pollution, offering a form of environmental resilience that public health advocates have long hypothesized but rarely demonstrated with prospective cohort data.

The associations were not uniform across the population. The positive relationships between air pollution and substance use disorder risk were most pronounced among males, participants aged 65 and older, and individuals with a history of smoking. These findings highlight the importance of considering demographic and behavioral modifiers when assessing the health consequences of environmental exposures, and they suggest that certain subgroups may benefit disproportionately from interventions aimed at reducing pollution or increasing green cover.

To ensure the robustness of their findings, the team conducted a series of sensitivity analyses. These included restricting the sample to long-term residents to minimize exposure misclassification from relocation, using alternative outcome definitions based on ICD-10 codes F10-F19 and F11-F19 to capture different ranges of substance-related diagnoses, and recomputing greenness measures at a wider 1000-meter buffer around each residence. The core conclusions held across these variations, strengthening confidence in the results.

The study was performed in accordance with the ethical principles of the Declaration of Helsinki and was registered with the UK Biobank under application number 46478. Ethical approval for the UK Biobank was granted by the North West Multi-centre Research Ethics Committee under approval reference 11/NW/0382. All participants provided written informed consent before any study-related procedures were initiated.

The work was supported by the China Postdoctoral Science Foundation, the Natural Science Basic Research Plan in Shaanxi Province of China, and the Fundamental Research Funds for the Central Universities. Corresponding authors are Bolun Cheng and Feng Zhang, both affiliated with Xi’an Jiaotong University, with Zhang also holding a position in the Department of Psychiatry at the First Affiliated Hospital of Xi’an Jiaotong University.

The findings come amid growing scientific interest in the neurological and psychiatric consequences of air pollution. Particulate matter, particularly PM2.5, is small enough to cross the blood-brain barrier and has been implicated in neuroinflammation, oxidative stress, and alterations in brain structure and function. These biological mechanisms could plausibly influence reward processing, impulse control, and stress reactivity, all of which are central to the development and perpetuation of substance use disorders.

Conversely, greenness has been associated with stress reduction, improved mental well-being, greater opportunities for physical activity and social interaction, and lower levels of psychological distress, each of which may buffer against the onset of addictive behaviors. The current study adds a significant piece of evidence to this emerging picture by demonstrating the relationship prospectively in one of the world’s largest and most deeply phenotyped biobanks.

The authors conclude that long-term exposure to ambient air pollutants was associated with a higher risk of incident substance use disorders and that residential greenness showed protective associations, with the most pronounced patterns observed among older males and individuals with a smoking history. They argue that the findings support integrating greenness exposure into environmental frameworks for the prevention of substance use disorders, a recommendation that carries implications for urban design, housing policy, and environmental regulation.

As cities around the world continue to grapple with the twin challenges of air quality and mental health, studies of this scale provide an evidence base for interventions that address both simultaneously. The prospect that something as tangible as a garden could offer measurable protection against the psychiatric consequences of polluted air adds a compelling dimension to ongoing debates about how the environments we build shape the minds that inhabit them.

The article is published open access under a Creative Commons Attribution 4.0 International License, permitting broad sharing and adaptation with appropriate credit to the original authors and source. It was received on 08 December 2025, accepted on 28 August 2026, and published on 09 September 2026.

In one of the most comprehensive investigations of its kind, researchers have taken a major step toward untangling the biology underlying suicide risk, moving the field beyond long-standing debates about whether suicidal behavior is simply a consequence of psychiatric illness. By integrating large-scale genetic data with cutting-edge approaches that map how genes act in specific brain cells and circuits, an international team has identified shared genetic liability that cuts across psychiatric diagnoses while also pinpointing druggable biological pathways that could one day inform prevention strategies. The study, published in Translational Psychiatry, offers a sweeping synthesis of how inherited risk factors may translate into molecular vulnerabilities, and it does so with a level of resolution that previous candidate-gene approaches could never achieve.

Suicide remains one of the leading causes of death worldwide, claiming more than 700,000 lives each year according to global health estimates. Despite decades of research, clinical prediction remains stubbornly imprecise, and biological models of suicidal behavior have historically been hampered by small sample sizes, inconsistent findings, and a tendency to conflate suicide risk with the psychiatric disorders with which it so often co-occurs. Major depression, bipolar disorder, schizophrenia, and substance use disorders all carry elevated suicide risk, yet most people with these conditions never attempt suicide, while some individuals who die by suicide have no diagnosed psychiatric illness at all. This paradox has long suggested to researchers that suicidal behavior may possess partially distinct biological underpinnings, and the new study set out to test that hypothesis with unprecedented statistical power.

At the heart of the work lies genome-wide association study methodology, or GWAS, which scans hundreds of thousands to millions of genetic variants spread across the entire genome in very large groups of people, comparing individuals who have experienced suicidal thoughts or behaviors with those who have not. Each variant is tested for statistical association with the outcome, and the results can be combined into polygenic risk scores, numerical summaries of a person’s inherited liability based on the cumulative small effects of thousands of variants. Because no single common variant exerts a large effect, the field depends on aggregating data across massive biobanks and cohorts, a strategy that has only become feasible in the past decade as datasets containing hundreds of thousands of individuals became available.

The research team took particular care to address a central confound: psychiatric disorders themselves are highly heritable, and any genetic signal linked to suicide could simply reflect inherited liability to depression or schizophrenia rather than to suicide specifically. To disentangle this, the investigators applied sophisticated statistical techniques, including genetic correlation analysis and conditional modeling, which allow researchers to ask how much genetic overlap remains between suicidal behavior and psychiatric conditions after accounting for their shared heritability. Their findings revealed a complex architecture. Substantial genetic correlations confirmed that suicide risk shares a meaningful fraction of its inherited basis with major psychiatric disorders, supporting the idea of a common pool of genetic liability. Yet the analyses also uncovered signals that persisted beyond what could be explained by those disorders, pointing to biological mechanisms that may be more specific to the emergence of suicidal thoughts and actions.

A key conceptual innovation of the study is its framing of “shared genetic liability” as a bridge between diagnoses. Rather than treating suicide as an epiphenomenon of any single disorder, the researchers modeled it as a transdiagnostic phenomenon, one whose risk emerges partly from inherited vulnerabilities that cut across diagnostic categories. This perspective aligns with a growing movement in biological psychiatry that emphasizes symptom dimensions and mechanisms over traditional diagnostic boundaries. From this vantage point, the genetic variants that raise risk for depression, PTSD, and schizophrenia may do so partly because they converge on shared molecular pathways, and those same pathways may govern an individual’s threshold for suicidal crises regardless of which diagnosis they carry.

Identifying genetic variants, however, is only the first step. A GWAS signal typically points to a genomic region rather than a specific causal gene or mechanism, since many associated variants fall in non-coding stretches of DNA that regulate gene activity from a distance. To translate statistical associations into biological insight, the team deployed a battery of functional genomics approaches. Transcriptome-wide association studies, known as TWAS, integrate gene expression data to identify genes whose genetically predicted expression levels are linked to suicide risk. Tissue and cell-type enrichment analyses then ask whether the implicated genes are unusually active in particular organs or cell populations. The results converged strikingly on brain tissue, and more specifically on neuronal populations, providing support for the idea that inherited suicide risk is mediated largely through gene regulation within the central nervous system.

The study’s most clinically provocative findings concern druggable biology. Using databases that catalog the protein targets of approved and investigational medications, the researchers examined whether genes implicated in suicide risk were over-represented among known drug targets. The analysis identified several classes of candidate targets, including components of neurotransmitter signaling systems, ion channels, and intracellular signaling cascades that are already the focus of pharmacological development for other conditions. This “druggable genome” approach, which has gained traction in genetics research across many diseases, offers a pragmatic shortcut for translational science: rather than waiting decades for entirely new therapeutic classes to be invented, researchers can prioritize existing or in-development compounds whose molecular targets intersect with genetically implicated pathways.

Among the pathways receiving attention in the analysis were those involving glutamatergic and GABAergic neurotransmission, the primary excitatory and inhibitory systems of the brain, which have repeatedly surfaced in studies of mood disorders and stress response. The endocannabinoid system and inflammatory signaling pathways also appeared in the convergent analyses, consistent with a broader literature linking immune dysregulation and allostatic load to suicidal ideation. Importantly, the authors emphasize that these findings identify hypotheses rather than ready-made treatments. Genetic association with a drug target does not guarantee that modulating that target will reduce suicide risk, and any therapeutic application would require extensive preclinical validation and carefully designed clinical trials. Nevertheless, the work provides a principled, data-driven map for where to look, replacing decades of largely failed candidate-gene speculation with a genome-wide evidence base.

The methodological rigor underpinning the study deserves emphasis, because the genetics of suicidal behavior has a troubled history. Early candidate-gene studies, which typically examined a handful of variants in genes related to serotonin signaling, produced findings that largely failed to replicate and in some cases were later shown to reflect statistical artifacts, small samples, and publication bias. The field has since undergone a reckoning, and modern efforts adhere to far stricter standards: preregistered analyses, very large and ancestrally diverse cohorts, replication in independent samples, and conservative multiple-testing corrections that demand genome-wide significance thresholds on the order of five times ten to the negative eighth power. The new study reflects these lessons, applying sensitivity analyses to guard against confounding from psychiatric comorbidity and examining whether findings generalize across ancestral groups, an issue of considerable importance given that most genetic discovery to date has been conducted in populations of European ancestry.

The implications for clinical practice, while still distant, are worth considering. Polygenic risk scores for suicide-related outcomes currently explain only a small fraction of individual differences in risk, far too little to be used as stand-alone screening tools, and their predictive performance is degraded in populations not represented in the discovery data. Researchers in the field are careful to stress that genetic risk is not destiny: suicidal behavior arises from an intricate interplay of inherited vulnerability, mental illness, trauma, substance use, social isolation, access to lethal means, and the availability of support. What genetics offers is not a crystal ball but a window into mechanism, and mechanistic knowledge is the raw material from which better biomarkers, risk stratification tools, and ultimately targeted interventions are built. In the near term, the druggable pathway findings are most valuable as a guide for laboratory science, directing neurobiologists toward molecular systems whose manipulation might alter suicide-relevant phenotypes in animal models and cellular assays.

Looking forward, the study signals where the field must go next. Sample sizes for suicide-specific genetic analyses remain smaller than those for major psychiatric disorders, and expanding representation across ancestries is essential if the benefits of this research are to be shared equitably. Integrating genetic data with longitudinal measures of life stress, neural imaging, and digital phenotyping may eventually allow researchers to model how inherited liability interacts with environmental triggers across the lifespan. Functional experiments in induced pluripotent stem cell-derived neurons and brain organoids could test whether the implicated genes genuinely alter stress-response circuitry or resilience. And randomized trials in patients carrying high genetic liability, though ethically and logistically complex, represent the logical endpoint of the druggable-target approach.

What the study ultimately delivers is a reframe. Suicide risk, in this analysis, is not an amorphous clinical outcome but a measurable, partly heritable trait whose genetic architecture is now being resolved with the same tools that have transformed our understanding of heart disease, diabetes, and schizophrenia. By demonstrating that shared genetic liability links suicide risk across diagnostic boundaries and by mapping that liability onto specific, pharmacologically tractable biology, the researchers have converted a long-standing clinical puzzle into a concrete research agenda. The path from genetic correlation to effective prevention is long, and no genetic finding will soon replace the human work of crisis intervention, connection, and care. But for a problem that has defied biological explanation for generations, the identification of shared, druggable mechanisms represents a genuine and hard-won advance, one that may shape suicide research for years to come.

Nearly every displaced woman in Gaza surveyed in a new study screened positive for severe post-traumatic stress symptoms, a finding researchers describe as an unprecedented psychological toll linked directly to hunger, overcrowded displacement, and the collapse of everyday life under war.

The study, published in the International Journal for Equity in Health, assessed 503 displaced women in the Gaza Strip during the 2023–2025 war using a mixed-methods design that combined a structured quantitative survey with in-depth qualitative interviews. The average participant was 29.4 years old, with a standard deviation of 7.3 years, and the majority were married, unemployed, and living below the deep poverty line. Most had been displaced for nearly a year, and the overwhelming majority were sheltering in tents under conditions of severe overcrowding and acute food shortage.

When researchers measured post-traumatic stress symptoms using the Impact of Event Scale–Revised, a widely used screening instrument that evaluates intrusion, avoidance, and hyperarousal symptoms following traumatic exposure, they found that 98.2 percent of participants scored in the severe range. The mean IES-R score across the sample was 61.5, with a standard deviation of 9.5 — a figure far above the thresholds typically used to flag clinically significant trauma-related distress. The authors are careful to note that because symptoms were assessed with a screening tool rather than a formal diagnostic clinical interview, the results should be interpreted as reflecting an extremely high burden of trauma-related distress within the study sample rather than confirmed clinical diagnoses. Even with that caveat, the near-universality of severe scores stands out even against the backdrop of other conflict-affected populations, where severe symptom prevalence rarely approaches such levels.

Food emerged as one of the strongest statistical correlates of psychological suffering. Severe food insecurity, measured with the Food Insecurity Experience Scale developed by the Food and Agriculture Organization, affected approximately 71 percent of participants. Women experiencing severe food insecurity had significantly higher PTSD symptom severity scores, an association that held at a p-value below 0.001. The researchers also identified a cluster of socioeconomic and living-condition factors associated with worse outcomes: being divorced or widowed, living in an extended-family household, sheltering in a tent or collective shelter during displacement, and reporting that food was simply unavailable were all significantly linked to elevated symptom scores.

These quantitative patterns were given texture and depth by the qualitative arm of the study, in which trained researchers conducted semi-structured, face-to-face interviews in Arabic with 34 of the women. Analysis of the transcripts revealed five overarching themes: poverty and inequity; food as a luxury; wounds you cannot see; on the move, nowhere to belong; and small acts of resilience. Together, the themes trace an arc from material deprivation to psychological injury and, ultimately, to the fragile coping strategies women deployed to keep themselves and their families functioning.

The theme of food as a luxury captured how a basic biological need had been transformed into an object of obsession and grief. Women described rationing scraps, skipping meals so children could eat, and the humiliating experience of standing in lines for aid that never arrived. The researchers note that this chronic preoccupation with food security operated on two fronts — it was simultaneously a source of traumatic stress in its own right and an amplifier of existing war trauma, since hunger stripped away one of the last remaining domains in which mothers could still protect their children.

The “wounds you cannot see” theme speaks directly to the invisible nature of psychological injury in wartime. Women recounted nightmares, intrusive memories of bombings and the deaths of relatives, hypervigilance, emotional numbness, and an inability to feel safe even in moments of quiet. Several described the stigma of admitting psychological suffering, or the sense that mental distress was a luxury they could not afford to acknowledge while survival demanded constant action. The researchers interpret these accounts as illustrating how trauma in this context is not a discrete event but a continuous condition, woven into the fabric of daily life.

Displacement itself — the theme of being “on the move, nowhere to belong” — emerged as a distinct psychological stressor. Women described repeated forced evacuations, the loss of homes that anchored family identity and memory, and the corrosive instability of living in tents that leaked in rain, baked in heat, and offered no privacy for grieving or for motherhood. The loss of place, the authors suggest, compounds the loss of people, producing a grief that has nowhere to settle.

Yet the final theme, small acts of resilience, complicates a narrative of pure victimhood. Women described prayer, mutual aid among neighbors, storytelling with children, and small rituals of domesticity — making tea, arranging a tent, celebrating a birthday with almost nothing — as deliberate acts of psychological resistance. The researchers frame these behaviors as adaptive coping mechanisms that, while insufficient to protect against severe trauma symptoms, sustained a sense of agency and dignity under conditions designed to strip both away.

Methodologically, the study relied on a convenience sample recruited through structured surveys administered via Google Forms, a pragmatic choice given the destruction of infrastructure and the impossibility of random sampling in an active war zone. The authors acknowledge this limitation, along with the screening-based measurement of PTSD and the absence of consistent formal referral pathways for psychological care during data collection, which meant that women who became distressed during interviews could not always be directed to clinical services. Interviews followed strict ethical protocols approved by the Institutional Review Board at An-Najah National University, with verbal informed consent, anonymization, and trained interviewers instructed to pause or terminate any conversation that caused visible distress.

The demographic profile of the sample underscores the socioeconomic dimension of psychological vulnerability. That most participants were unemployed and living below the deep poverty line before and during the war reflects broader patterns in which economic deprivation and mental health outcomes are tightly intertwined in conflict settings. Divorced and widowed women — those without a partner’s social and economic support — fared significantly worse, as did women in extended-family households, possibly reflecting crowded conditions and multiplied caregiving burdens.

The study carries a sobering human footnote. The acknowledgments honor the memory of co-author Ayman S. Abutair, a clinical nutrition researcher at Al-Azhar University-Gaza, who lost his life during the war before the paper’s publication. His death stands as a stark reminder that the researchers documenting these invisible wounds were themselves living within the same catastrophe.

The authors argue that their findings demonstrate an urgent and unmet need for comprehensive humanitarian and psychosocial support tailored to displaced women — support that integrates mental health care with food assistance, shelter improvement, and protection for female-headed households. They emphasize that because caregiving responsibilities fall disproportionately on women during war and displacement, their psychological deterioration radiates outward to children and entire family systems, making women’s mental health a strategic priority for any humanitarian response rather than an afterthought.

What the study ultimately documents is the entanglement of hunger and trauma at a scale rarely captured in research. Where most studies of conflict-related PTSD examine populations after violence has subsided, this research measured psychological injury while bombs were still falling, while displacement was ongoing, and while food systems had collapsed. The result is a portrait of a population in which severe trauma symptoms are not an unfortunate consequence of war but, in effect, a near-universal condition — visible not in wounds, but in sleepless nights, interrupted meals, and the quiet endurance of half a million women carrying burdens that remain, for now, largely untreated.

Police have finally dropped a year-long investigation into three hero passengers who tackled a man exposing himself in front of children on a train – though only because the CPS has refused to take the case forward.

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A new study published in Risk Analysis found that residents living within five miles of the former Santa Susana Field Laboratory reported autoimmune disorders at more than four times the rate of those living 11 to 15 miles away.

Researchers from the University of Southern California led the study, shifting focus beyond the cancer statistics that have dominated discussion of the site for years. Instead, they examined health conditions and protective behavior among residents of a higher-income community living near a contaminated site, rather than the lower-income communities typically studied in environmental risk research.

An Unused Meltdown Superfund

Located in the Simi Hills northwest of Los Angeles, the Santa Susana Field Laboratory hosted rocket engine testing from 1949 to 2006 and nuclear reactor operations from 1953 to 1980. In 1959, a partial meltdown occurred at the site, which later became associated with radioactive and chemical contamination in soil and groundwater both on and beyond the property. Some have described the accident as the worst nuclear accident in U.S. history.

Although SSFL was designated a Superfund-eligible site in 1989, it has never been added to the National Priorities List. As a result, the site has not been cleaned up through the standard federal Superfund process.

Previous health studies did not find a significant increase in most cancers among those who lived near the site. A 1992 California Department of Health Services report also concluded that people living near SSFL were not at increased risk of developing cancers associated with radiation exposure. However, many residents and advocacy groups still believe that contamination from the Santa Susana Field Laboratory may be negatively impacting community health.

Testing What Money Can and Can’t Buy

Most Superfund sites are located in low-income areas, with 62% of nearby households earning less than $50,000 a year nationwide. The Santa Susana Field Laboratory is different, as it is surrounded by higher-income neighborhoods. This gave the USC team an opportunity to examine how residents with greater financial resources respond to environmental hazards in their community.

Led by Jenna Blyler of the USC Wrigley Institute for Environment and Sustainability, the team surveyed 475 residents living within 15 miles of the site. More than half (56%) reported household incomes of $100,000 or more.

Illness That Tracks With Distance

The study found that 18% of residents living within five miles of the Santa Susana Field Laboratory reported autoimmune disorders, as compared to 4% of those living between 11 and 15 miles from it. Similarly, 15% of residents living within five miles reported metabolic and endocrine disorders, compared with 2% of those living 11 to 15 miles away.

Over one third of residents said they had received at least one chronic diagnosis since moving to the area, a rate similar to the national average of 38%. This result is notable because chronic illness is usually less common in higher-income communities.

Fear as a Motivator

“We expected to see wealthier people take more actions to protect themselves given their greater capacity to cope and affect change,” Blyler said. “Instead, fear of the contamination was what motivated protective action, rather than their perceived ability to manage the risks.”

The study also found that residents were more likely to adopt protective measures if they believed those measures were expensive. The finding runs counter to the researchers’ expectations and to previous research suggesting that higher costs can discourage protective behavior.

Blyler and her coauthor, Joseph Árvai, suggest two possible reasons for this result. The community may be able to afford costs that would prevent other groups from taking action, or residents may see a higher price as a sign that a precaution is effective and worth the investment.

What the Study Can’t Answer

The authors note several limitations of the study. The research is based on self-reported diagnoses collected at one point in time, and it does not show that contamination from the Santa Susana Field Laboratory directly caused the health conditions residents reported.

The researchers also found that health anxiety partially explained the relationship between existing illness and protective behavior, but the study could not determine why certain conditions were more frequently reported closer to SSFL.

Future studies using objective health data and longer-term follow-up could help determine whether the reported patterns reflect actual differences in disease prevalence and whether environmental exposure plays a role.

Austin Burgess is a writer and researcher with a background in sales, marketing, and data analytics. He holds an MBA, a Bachelor of Science in Business Administration, and a data analytics certification. His work focuses on breaking scientific developments, with an emphasis on emerging biology, cognitive neuroscience, and archaeological discoveries.

The Federal Bureau of Investigation looks almost unrecognizable under director Kash Patel’s leadership.

The agency’s head has been embroiled in a seemingly endless list of controversies, from allegations of excessive drinking to buying up location data on everyday American citizens to furthering of harebrained conspiracies.

Patel lacked virtually any degree of relevant working experience for the job before the Senate confirmed him — and now, the agency is opening the doors for even more highly questionable hirings.

As inside sources told CBS News, the FBI has quietly lowered standards of its background checks for potential federal agents and other personnel. The bureau is now officially looking the other way when it comes to prostitution, for instance — as long as recruits didn’t hire sex workers over three times.

Even more eyebrow-raising is that the FBI is even allowing the consideration of candidates who engaged in bestiality or animal cruelty, according to CBS‘ sources. However, any such incidents would’ve had to have taken place before the candidate turned 18.

The broadcaster’s sources also said there was no distinction between candidates who were forced into sexual activity with animals or if they did so willingly. An FBI spokesperson claimed that eligibility requirements were limited to a “narrow set of circumstances, such as in cases where a person was sexually abused with animals as a child.”

Experts, however, were appalled at the news, arguing that the FBI is undermining its responsibility in vetting applicants by changing background check standards.

“Bestiality is clearly a potential indication of a more serious emotional issue, and even in a circumstance where it is not, the pool of candidates should be extensive enough that the criteria should certainly not be eliminated,” former FBI agent James Davidson told CBS.

Before the changes, which were reportedly implemented earlier this summer, the FBI’s webpage was clear about automatically disqualifying special agents who engaged in “prostitution or bestiality.”

Both current and former FBI employees told the CBS that the bureau could now be hiring “people with questionable backgrounds,” allowing them to undermine the integrity of the service. Others warned that the news was evidence of a major “recruiting problem.”

Considering the fact that the agency is being helmed by a personality as controversial as Patel, these changes shouldn’t come as too much of a shock.

While he hasn’t personally acknowledged the latest changes, Patel has frequently called for new hiring standards at the bureau, arguing that “we are losing too many qualified candidates to the rigors of the requirements from yesteryear” in a July interview with former FBI agent John Nantz.

Patel’s motivation for lowering standards could be to bring in his closest associates. As ProPublica reported in November, his personal assistant didn’t clear their polygraph test and required a waiver, claims the FBI has since denied.

More on Patel: The Head of the FBI Just Admitted Something Moderately Horrifying

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