Modern life runs on chemistry and, most of the time, that’s a good thing. It’s what allows us to treat disease, preserve food, purify water, and build the materials we rely on every day. But the widespread use of synthetic chemicals also means some exposures have outpaced our understanding of their long-term effects on human health.
This complexity is reflected in how cancer risk is communicated. When the World Health Organization’s International Agency for Research on Cancer (IARC) classified processed meat, such as bacon and sausages, as a Group 1 carcinogen in 2015, the announcement generated global headlines, and continues to be widely cited in discussions of cancer risk today. It also generated an obvious question: if these products are carcinogenic, why are they still so widely consumed and not subject to the same restrictions as tobacco or asbestos?
The answer lies in what IARC classifications are designed to convey: they reflect the strength of the evidence that an agent can cause cancer under some conditions, not the magnitude or risk under typical patterns of exposure. As a foundational principle of toxicology, risk depends not simply on whether a hazard exists, but on the nature, duration, and level of exposure (colloquially, “the dose makes the poison”). In other words, not all Group 1 carcinogens carry the same level of risk in everyday life. Regulatory decisions therefore consider not only whether an agent can cause cancer, but also how people are exposed, at what levels, and whether these exposures can be meaningfully reduced.
Here’s a grounded way to think about it: not all chemicals are equal, and not all evidence is equal. Some agents have strong human data; others have mechanistic red flags and early epidemiology; and many sit in a gray zone. Independent organizations such as IARC and national regulatory agencies systematically evaluate this evidence, and their assessments provide the most reliable reference point interpreting carcinogenic risk and exposure. This evidence reinforces a simple principle: where credible evidence of carcinogenicity exists, minimizing unnecessary exposure is a prudent and responsible approach, even as scientific understanding continues to evolve.
Where the evidence is strongest
Formaldehyde and formaldehyde-releasing preservatives (e.g. Quaternium-15; DMDM Hydantoin; imidazolidinyl, diazolidinyl or polyoxymethylene urea), commonly used to extend the shelf life of certain personal care products (including lotions, baby shampoo, soaps, cosmetics, hair-smoothing treatments, and even eyelash glue), in composite wood and fertilizers, are known human carcinogens linked to nasopharyngeal cancer and leukemia, especially when exposure involves inhalation in poorly ventilated settings[1]. The European Union (EU) has banned formaldehyde in cosmetics on this basis, whereas in the United States its use is still permitted in some products under concentration and exposure limits.
Talc contaminated with asbestos, historically used in certain baby and body powders, and in cosmetic products, is a known human carcinogen due to the presence of asbestos fibers, which are causally linked to ovarian cancer, mesothelioma, and lung cancer following long-term inhalation or perineal exposure[2]. While cosmetic-grade talc is now required to be asbestos-free in many jurisdictions, contamination has been documented in some products, prompting increased regulatory scrutiny[3]. In the United States, talc-containing products remain available, though several manufacturers have withdrawn talc-based formulations from the market in recent years as a result of litigation pressures[4].
Benzene, a volatile organic compound present in gasoline fumes, vehicle exhaust and tobacco smoke, is also found in range of household products, including detergents, degreasers and aerosol sprays, paints and paint thinners, adhesives, and stored fuels such as petrol for lawnmowers. While occupational exposure has historically posed the highest risk, environmental exposure contributes to cumulative lifetime dose. Whereas the EU restricts benzene content in consumer products and fuels to very low levels, in the United States benzene remains present in gasoline and has been intermittently detected in drugs and certain consumer products, including aerosols and personal care items[5].
Where the evidence is concerning but more variable
Per- and polyfluoroalkyl substances (PFAS; “forever chemicals”), used for stain-, water-, and grease-resistance in items like textiles, cookware coatings, and food packaging, are highly persistent and can accumulate in the body. IARC has classified one widely studied PFAS, perfluorooctanoic acid (PFOA; previously used in nonstick cookware, microwave popcorn bags, fast-food wrappers and pizza boxes) as carcinogenic to humans. This classification is based on sufficient evidence for kidney cancer and limited evidence for testicular cancer[6]. Although many uses have been phased out, PFOS is highly persistent and can remain in the environment and as a trace contaminant long after its production and use have ceased. IARC also emphasizes that carcinogenic risk varies across different PFAS compounds, exposure levels, and populations.
Parabens and phthalates, widely used preservatives in personal care products, food, and some packaging, have attracted scientific attention because studies show they can interfere with hormone signaling, including weakly mimicking estrogen[7]. Many readers will be familiar with parabens from the now-common “paraben-free” labels found on skincare and cosmetic products, reflecting their widespread use and ongoing scientific scrutiny. IARC notes that parabens exhibit key characteristics of carcinogens in experimental systems and can stimulate breast cancer growth in laboratory models, although carcinogenicity has not yet been conclusively demonstrated in humans or experimental animals. Based on widespread exposure and available mechanistic evidence, IARC has identified parabens as high-priority agents for future evaluation, and their long-term cancer risk continues to be assessed[8]. Related endocrine-active chemicals, including phthalates and bisphenols, are also encountered through everyday sources such as personal care products, thermal paper receipts, and some menstrual products, including tampons and pads, where trace levels have been detected. Intervention studies show that use of selected personal care products can lower biomarkers of exposure and alter gene expression patterns in breast tissue, highlighting the biological relevance of these exposures and the need for continued evaluation[9, 10].
Bisphenol (BPA), used in polycarbonate plastics and epoxy resins and found in food containers, reusable bottles, canned food and beverage linings, has raised concern because it acts as an endocrine disruptor, with some studies linking it to hormone-related cancers, such as breast and prostate cancers[11]. The use of BPA has declined substantially in recent years; the EU has banned BPA in food contact materials, with phased implementation beginning in 2025, while in the United States it has already been removed from baby bottles and infant formula packaging, although it remains permitted in certain other regulated applications, including resins used in food and beverage can coatings[12, 13]. IARC has not yet classified BPA as carcinogenic to humans but has designated it a high-priority agent for evaluation, citing mechanistic evidence relevant to tumor development alongside inconclusive epidemiological findings in humans[8].
Where the evidence remains uncertain, and how to interpret it responsibly
Aluminium salts, the active ingredients in antiperspirants, have attracted scrutiny because laboratory studies suggest they can interact with hormone-related pathways and be absorbed in trace amounts through the skin. However, epidemiological evidence linking antiperspirant use to breast cancer remains inconclusive, and IARC reports that there is currently no convincing evidence that aluminium exposure causes cancer in humans or experimental animals[8]. Aluminium production as an industrial process has been classified as carcinogenic to humans, but this risk is attributed primarily to co-exposure to other carcinogens, such as polycyclic aromatic hydrocarbons, rather than aluminium metal. Reflecting these distinctions, IARC has concluded that a formal carcinogenicity evaluation of aluminium is unwarranted at this stage, highlighting the importance of distinguishing between hazard signals, exposure context, and demonstrated cancer risk when communicating evidence responsibly.
Artificial sweeteners, familiar to many consumers through “diet” and “zero-sugar” sweet beverages, have come under scrutiny following recent evaluations of aspartame, one of the most widely used compounds in this class. Aspartame has been classified by IARC as possibly carcinogenic to humans (Group 2B), a category used when limited evidence suggests a potential hazard but does not establish that the substance causes cancer under typical exposure conditions[8]. Global food safety authorities, including the WHO and Joint FAO/WHO Expert Committee on Food Additives, continue to consider aspartame safe within established intake limits. Reflecting this, IARC has identified sugar-sweetened beverages (not artificially-sweetened beverages) as a higher priority for future carcinogenicity evaluation, underscoring the importance of considering alternatives to excess sugar intake in the broader context of cancer risk. These distinctions highlight the importance of interpreting carcinogenicity classifications alongside the strength of evidence and real-world exposure data, rather than viewing them as definitive measures of cancer risk.
Radiofrequency electromagnetic fields (RF-EMF), emitted by devices such as mobile phones, Wi-Fi routers, and other wireless Bluetooth devices including earbuds, have previously been classified by IARC as possibly carcinogenic to humans (Group 2B), based on limited evidence for glioma and acoustic neuroma in heavy mobile phone users. Since that classification, additional high-quality studies have produced mixed results in humans, alongside new evidence of carcinogenicity in experimental animals and mechanistic findings that remain inconsistent[8]. Reflecting this evolving evidence base, IARC has designated RF-EMF a high priority for re-evaluation, while noting that whether the current classification will change remains uncertain. In practice, this means RF-EMF remains an area of scientific uncertainty: whereas existing evidence does not confirm that typical wireless device use causes cancer, it warrants continued study.
Unpacking exposure: Duration, dose, and biological plausibility
Cancer risk depends not just on whether a substance can cause harm, but on how, how much, and for how long exposure occurs. In this context, three factors are central: duration, dose, and biological plausibility[14]:
Duration: how long are you exposed?
Cancer is typically the result of long-term biological change, not a single moment. For example, lung cancer risk rises with cumulative tobacco, radon or air pollution exposure over years or decades, reflecting the gradual accumulation of DNA damage. While acute, high-intensity exposures can be important for some carcinogens (such as ionizing radiation from nuclear accidents or medical overexposure), sustained exposure over years or decades is what most often shapes population-level risk. Timing can also matter: exposures during periods of rapid development, such as in early life, may have different consequences than exposures later in life. Children exposed to ionizing radiation, for example, have a substantially higher lifetime risk of certain cancers than adults exposed at the same dose, underscoring how biological vulnerability can change across the lifespan[15].
Dose: how much actually reaches the body?
Dose begins with what a product contains, but risk depends on the concentration of the carcinogen and how much of it enters the body over time. The same substance can pose very different risks depending on how and how much it is used.
For example, formaldehyde may be present in some cosmetics, personal care products, and composite wood materials, resulting in repeated low-level exposure through skin contact or indoor air. Certain hair-smoothing treatments (including some keratin-based formulations) can release higher concentrations into the air during use, particularly when heat is applied, increasing inhalation exposure[16]. In both cases, the carcinogen is the same, but concentration, frequency, and route of exposure together determine cumulative dose and how much reaches biologically relevant tissues. This is why factors such as ventilation, heating, repeated use, and duration of exposure play a critical role in determining risk.
Biological plausibility: is there a credible mechanism?
Biological plausibility asks a simple question: is there a scientifically credible way this exposure could contribute to cancer? Carcinogens often act through multiple biological mechanisms, including damaging DNA, altering gene regulation, suppressing immune surveillance, or modulating receptor-mediated pathways, processes that can ultimately lead to the cellular changes required for cancer development[17]. For example, BPA can bind to hormone receptors and alter gene expression in experimental systems, providing a biologically plausible pathway through which it could influence cancer development. However, demonstrating a mechanism is only one part of understanding risk.
Taken together, these three factors (duration, dose and biological plausibility) help explain why some exposures increase cancer risk while others do not. A carcinogen must not only have a credible biological mechanism, but also reach the body in sufficient amounts and over sufficient time to cause harm.
At the same time, the absence of definitive evidence in one area does not mean that a substance is safe: many exposures initially raise concern based on mechanistic or early epidemiological findings, and are only confirmed as carcinogenic after years of accumulated research. Cancer risk assessment is therefore an evolving process, shaped by the gradual convergence of mechanistic, experimental, and human evidence.
Evidence over hype: How to avoid being misled
Most carcinogenicity evaluations today, particularly those conducted by independent scientific bodies such as IARC, the World Health Organization (WHO), and national health agencies, are based on transparent review of publicly available evidence and strict conflict-of-interest safeguards. These evaluations are updated periodically as new data emerge and represent the most reliable reference point for understanding cancer risk. At the same time, public skepticism about carcinogens is shaped in part by historical cases, such as tobacco and asbestos, where evidence of harm emerged well before regulatory action and, in some instances, was actively challenged or downplayed by affected industries.
Because evaluations are conducted independently of the industries that manufacture or use these substances, understanding how scientific bodies assess evidence can help clarify what their conclusions mean in practice:
What kind of evidence is this based on?
Stronger conclusions are supported by consistent findings from human studies, alongside animal and mechanistic research. Early laboratory and animal findings are often the first signal of concern, but do not always translate directly to human risk. For example, some animal studies have reported increased tumor rates with very high doses or aspartame, but large human cohort studies have not shown consistent associations with cancer, and global health authorities continue to consider it to be safe within recommended intake limits[18].
Has the finding been replicated?
Confidence increases when multiple independent studies reach similar conclusions over time. However, lack of replication does not mean an exposure is safe; it may reflect the time required to study long-term effects or challenges in measuring exposure. This is why independent scientific bodies periodically reassess risks as new evidence becomes available.
Is there evidence of dose-response relationship?
Cancer risk typically increases with greater or longer exposure. This helps explain why agencies consider not just whether a substance can cause cancer, but at what levels and under what conditions risk has been observed. Reducing cumulative exposure to established carcinogens (including formaldehyde, benzene, and PFAS), remains a cornerstone of cancer prevention.
What do independent expert bodies conclude overall?
Agency classifications reflect evaluation of the totality of evidence (including human, animal and mechanistic studies), rather than individual findings in isolation. These conclusions provide the most dependable basis for understanding whether an exposure is known to cause cancer, suspected to do so, or still under investigation.
Is the evidence still evolving?
Some exposures, such as RF-EMF from wireless devices, remain under active investigation. A “possible carcinogen” classification reflects limited evidence and scientific uncertainty; it does not mean cancer risk is proven, but it also does not confirm safety. In these cases, it is prudent to follow updates from independent health agencies and, where possible, to take simple steps to reduce unnecessary exposure while scientific understanding advances.
Informed, not alarmed
Cancer risk is rarely defined by a single exposure, product, or moment. More often, it reflects the cumulative effects of biology, environment, and time. Understanding how carcinogens are identified, and how duration, dose, and biological plausibility interact, helps move the conversation beyond headlines toward evidence.
Independent scientific agencies provide the most reliable framework for interpreting this evolving knowledge. Their conclusions do not eliminate uncertainty, but they allow individuals, clinicians, and policymakers to make informed decisions grounded in the best available science.
For individuals, the goal is not to eliminate every theoretical risk (an impossible task), but to reduce avoidable exposures where credible evidence exists, particularly when safer alternatives are readily available. Small, consistent reductions in cumulative exposure can meaningfully shift risk over a lifetime.
For us at Helix BioPharma, this question is not abstract. Cancer prevention and treatment both begin with understanding the biological mechanisms that drive disease, and using that knowledge to intervene more effectively. Whether developing new therapies or communicating emerging science, our responsibility is the same: to follow the evidence, wherever it leads, and to help translate it into progress. Because, ultimately, the most powerful tool in reducing cancer risk is not fear, but knowledge.
References:
1. Eftekhari, A., Won, Y., Morrison, G., & Ng, N. L. (2023). Chemistry of indoor air pollution. American Chemical Society.
2. Singh, S., Pradhan, S. R., Yadav, A., & Singh, P. K. (2023). Banning asbestos in talcum powder: Time for action in India. Dialogues in Health, 3, 100158. doi: https://doi.org/10.1016/j.dialog.2023.100158
3. https://www.fda.gov/cosmetics/cosmetic-ingredients/talc
7. https://www.niehs.nih.gov/health/topics/agents/endocrine
8. https://monographs.iarc.who.int/wp-content/uploads/2024/11/AGP_Report_2025-2029.pdf
9. Alnuqaydan, A. M. (2024). The dark side of beauty: an in-depth analysis of the health hazards and toxicological impact of synthetic cosmetics and personal care products. Frontiers in public health, 12, 1439027. doi: https://doi.org/10.3389/fpubh.2024.1439027
10. Hassan, M. H., Nadeem, F., Asif, R., Ahmed, A., Ahmad, A. M., Junaid, G., … & Zaman, M. T. (2024). A Review on the Effects of Daily Use Chemicals on Human Health. Journal of Health and Rehabilitation Research, 4 (3), 1-8. doi: https://doi.org/10.61919/jhrr.v4i3.1803
11. https://link.springer.com/article/10.1007/s00420-021-01752-5
12. https://www.efsa.europa.eu/en/topics/topic/bisphenol
14. Donzelli, G., Gehring, R., Murugadoss, S., Roos, T., Schaffert, A., & Linzalone, N. (2025). A critical review on the toxicological and epidemiological evidence integration for assessing human health risks to environmental chemical exposures. Reviews on Environmental Health, 40 (2), 427-436. doi: https://doi.org/10.1515/reveh-2024-0072
15. https://publications.iarc.who.int/120
16. https://www.osha.gov/hair-salons