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Common environmental chemicals assumed to be safe at low doses may act separately or together to induce cancer development, according to research published in Carcinogenesis.
Investigators studied low-dose effects of 85 common chemicals not considered to be carcinogenic to humans, reviewing the actions of these chemicals against a long list of mechanisms that are important for cancer development.
The team compared the chemicals’ biological activity patterns to 11 known hallmarks of cancer—distinctive patterns of cellular and genetic disruption associated with early cancer development.
The chemicals included the pain reliever acetaminophen; bisphenol A (BPA), which is used in plastic food and beverage containers; rotenone, a broad-spectrum insecticide; paraquat, an agricultural herbicide; and triclosan, an antibacterial agent used in soaps and cosmetics.
The investigators learned that 50 of the 85 chemicals they analyzed can disrupt cell function in ways that correlate with known early patterns of cancer, even at the low, presumably benign levels at which most people are exposed.
For 13 of the chemicals, the team found evidence of a dose-response threshold—a level of exposure at which a chemical is considered toxic by regulators. For 22 chemicals, there was no toxicity information at all.
“Our findings also suggest these molecules may be acting in synergy to increase cancer activity,” said William Bisson, PhD, of Oregon State University in Corvallis.
“For example, EDTA, a metal-ion-binding compound used in manufacturing and medicine, interferes with the body’s repair of damaged genes. EDTA doesn’t cause genetic mutations itself, but if you’re exposed to it along with some substance that is mutagenic, it enhances the effect because it disrupts DNA repair, a key layer of cancer defense.”
Dr Bisson said the main purpose of this study was to highlight gaps in knowledge of environmentally influenced cancers and to set forth a research agenda for the next few years. He added that more research is still necessary to assess early exposure and to understand early stages of cancer development.
Traditional risk assessment, Dr Bisson said, has historically focused on a quest for single chemicals and single modes of action—approaches that may underestimate cancer risk. With this study, investigators took a different tack, examining the interplay over time of independent molecular processes triggered by low-dose exposures to chemicals.
“Cancer is a disease of diseases,” Dr Bisson said. “It follows multi-step development patterns, and, in most cases, it has a long latency period. It has to be tackled from an angle that considers the complexity of these patterns. A better understanding of what’s driving things to the point where they get uncontrollable will be key for the development of effective strategies for prevention and early detection.” 
Common environmental chemicals assumed to be safe at low doses may act separately or together to induce cancer development, according to research published in Carcinogenesis.
Investigators studied low-dose effects of 85 common chemicals not considered to be carcinogenic to humans, reviewing the actions of these chemicals against a long list of mechanisms that are important for cancer development.
The team compared the chemicals’ biological activity patterns to 11 known hallmarks of cancer—distinctive patterns of cellular and genetic disruption associated with early cancer development.
The chemicals included the pain reliever acetaminophen; bisphenol A (BPA), which is used in plastic food and beverage containers; rotenone, a broad-spectrum insecticide; paraquat, an agricultural herbicide; and triclosan, an antibacterial agent used in soaps and cosmetics.
The investigators learned that 50 of the 85 chemicals they analyzed can disrupt cell function in ways that correlate with known early patterns of cancer, even at the low, presumably benign levels at which most people are exposed.
For 13 of the chemicals, the team found evidence of a dose-response threshold—a level of exposure at which a chemical is considered toxic by regulators. For 22 chemicals, there was no toxicity information at all.
“Our findings also suggest these molecules may be acting in synergy to increase cancer activity,” said William Bisson, PhD, of Oregon State University in Corvallis.
“For example, EDTA, a metal-ion-binding compound used in manufacturing and medicine, interferes with the body’s repair of damaged genes. EDTA doesn’t cause genetic mutations itself, but if you’re exposed to it along with some substance that is mutagenic, it enhances the effect because it disrupts DNA repair, a key layer of cancer defense.”
Dr Bisson said the main purpose of this study was to highlight gaps in knowledge of environmentally influenced cancers and to set forth a research agenda for the next few years. He added that more research is still necessary to assess early exposure and to understand early stages of cancer development.
Traditional risk assessment, Dr Bisson said, has historically focused on a quest for single chemicals and single modes of action—approaches that may underestimate cancer risk. With this study, investigators took a different tack, examining the interplay over time of independent molecular processes triggered by low-dose exposures to chemicals.
“Cancer is a disease of diseases,” Dr Bisson said. “It follows multi-step development patterns, and, in most cases, it has a long latency period. It has to be tackled from an angle that considers the complexity of these patterns. A better understanding of what’s driving things to the point where they get uncontrollable will be key for the development of effective strategies for prevention and early detection.”
Common environmental chemicals assumed to be safe at low doses may act separately or together to induce cancer development, according to research published in Carcinogenesis.
Investigators studied low-dose effects of 85 common chemicals not considered to be carcinogenic to humans, reviewing the actions of these chemicals against a long list of mechanisms that are important for cancer development.
The team compared the chemicals’ biological activity patterns to 11 known hallmarks of cancer—distinctive patterns of cellular and genetic disruption associated with early cancer development.
The chemicals included the pain reliever acetaminophen; bisphenol A (BPA), which is used in plastic food and beverage containers; rotenone, a broad-spectrum insecticide; paraquat, an agricultural herbicide; and triclosan, an antibacterial agent used in soaps and cosmetics.
The investigators learned that 50 of the 85 chemicals they analyzed can disrupt cell function in ways that correlate with known early patterns of cancer, even at the low, presumably benign levels at which most people are exposed.
For 13 of the chemicals, the team found evidence of a dose-response threshold—a level of exposure at which a chemical is considered toxic by regulators. For 22 chemicals, there was no toxicity information at all.
“Our findings also suggest these molecules may be acting in synergy to increase cancer activity,” said William Bisson, PhD, of Oregon State University in Corvallis.
“For example, EDTA, a metal-ion-binding compound used in manufacturing and medicine, interferes with the body’s repair of damaged genes. EDTA doesn’t cause genetic mutations itself, but if you’re exposed to it along with some substance that is mutagenic, it enhances the effect because it disrupts DNA repair, a key layer of cancer defense.”
Dr Bisson said the main purpose of this study was to highlight gaps in knowledge of environmentally influenced cancers and to set forth a research agenda for the next few years. He added that more research is still necessary to assess early exposure and to understand early stages of cancer development.
Traditional risk assessment, Dr Bisson said, has historically focused on a quest for single chemicals and single modes of action—approaches that may underestimate cancer risk. With this study, investigators took a different tack, examining the interplay over time of independent molecular processes triggered by low-dose exposures to chemicals.
“Cancer is a disease of diseases,” Dr Bisson said. “It follows multi-step development patterns, and, in most cases, it has a long latency period. It has to be tackled from an angle that considers the complexity of these patterns. A better understanding of what’s driving things to the point where they get uncontrollable will be key for the development of effective strategies for prevention and early detection.”