Prostate cancer is the most common solid cancer in males and is the second leading cause of cancer deaths in American men Jemal et al. While rates today are markedly higher than rates observed three decades ago, the most recent statistics show that prostate cancer incidence rates have now stabilized which is thought to reflect changes in utilization of prostate-specific antigen PSA testing. Despite extensive research, the basis for these high rates of abnormal prostatic growth is not well understood. It is recognized, however, that steroids play a role in the initiation and progression of prostate cancer which is the basis for hormonal treatment strategies. Furthermore, it is believed that early prostatic developmental events which are regulated by steroids may be linked to the predisposition of this structure to high rates of disease in adult men Henderson et al.
J Neurochem. Please note the date Environmentsl last review on all articles. Psychol Methods. In addition to AR antagonistic effects Gray et al. Get medical imaging studies only when you need them. Toxicol Appl Pharmacol. J Korean Med Sci. This raises the possibility that the fetal prostate may be affected following maternal use of these compounds.
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The prostate is a small gland located underneath the bladder in men and is part of the reproductive system.
- Cancer is caused by changes to certain genes that alter the way our cells function.
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Prostate cancer is the most common solid cancer in males and is the second leading cause of cancer deaths in American men Jemal et al. While rates today are markedly higher than rates observed three decades ago, the most recent statistics show that prostate cancer incidence rates have now stabilized which is thought to reflect changes in utilization of prostate-specific antigen PSA testing.
Despite extensive research, the basis for these high rates of abnormal prostatic growth is not well understood. It is recognized, however, that steroids play a role in the initiation and progression of prostate cancer which is the basis for hormonal treatment strategies.
Furthermore, it is believed that early prostatic developmental events which are regulated by steroids may be linked to the predisposition of this structure to high rates of disease in adult men Henderson et al.
It is noteworthy that relative to adult estrogenic responses, the prostate gland is particularly sensitive to estrogen exposures during the critical developmental period Prins et al. The established risk factors for prostate cancer are age and race with African American men possessing the highest incidence of prostate cancer worldwide, at rates twofold of those for Caucasian-American counterparts. It is also recognized that genetics family history , diet, and environmental factors can impact prostate cancer risk.
In the human population, direct connections between endocrine disruptors EDs and prostate cancer risk have not been established. Nonetheless, due to the hormonal basis of this disease and the evidence that dietary compounds high in isoflavones e. Due to difficulties in directly associating prostate cancer risk in humans with ED exposures, potential risk s will have to include research with animal models, particularly those that that are responsive to environmentally relevant exposures.
Regarding links between prostate cancer and environmental factors in humans outside of diet , the most compelling data come from the established occupational hazard of farming and increased prostate cancer rates Morrison et al. While several variables may contribute to higher prostate cancer rates in farmers, chronic or intermittent exposures to pesticides are the most likely explanation Alavanja et al.
Furthermore, 6 pesticides out of 45 common agricultural pesticides showed correlation with exposure and increased prostate cancer in men with a familial history, suggesting gene—environment interactions.
These six agents were chlorpyrifos, fonofos, coumaphos, phorate, permethrin, and butylate Alavanja et al. The first four of these compounds are thiophosphates and share a common chemical structure. While these agents are regarded as acetylcholine esterase inhibitors and have not been shown to have direct estrogenic or anti-androgenic activities, a literature search revealed that these compounds have significant capacity as p enzyme inhibitors.
In particular, chlorpyrifos, fonofos, and phorate strongly inhibit CYP1A2 and CYP3A4 which are the major ps that metabolize estradiol, estrone, and testosterone in the liver Usmani et al. This raises the possibility that exposure to these compounds may interfere with steroid hormone metabolism by the liver as well as the prostate and, in so doing, alter steroid balance and availability which in turn may contribute to increased prostate cancer risk.
A similar mechanism of endocrine disruption in vivo has been identified for polychlorinated biphenols PCBs and polyhalogenated aromatic hydrocarbons including dioxins, bisphenol A BPA , and dibenzofurans through potent inhibition of estrogen sulfotransferase which effectively elevates bioavailable estrogens in various target organs Kester et al.
In men, chronically elevated estrogens have been associated with increased risk of prostate cancer Modugno et al. In rodents, estrogens in combination with androgens induce prostate cancer Leav et al. For the sake of simplicity, we here refer to environmental estrogens as molecules with identified estrogenic activity estrogen mimics , mostly through activation of ERs.
DES exposure is considered an important model of endocrine disruption and provides proof of principle for exogenous estrogenic agents as disruptors of multiple endorgans. While prostatic metaplasia eventually resolved following DES withdrawal, ectasia and persistent distortion of ductal architecture remained Yonemura et al. This has lead to the postulation that men exposed prenatally to DES may be at increased risk for prostatic disease later in life although this has not been borne out in the limited population studies conducted to date Giusti et al.
The effects of BPA with regard to carcinogenic potential, including the prostate gland, have recently been reviewed by an expert panel Keri et al. In short, there is evidence from rodent models and human prostate cell lines that BPA can influence carcinogenesis, modulate prostate cancer cell proliferation, and for some tumors, stimulate progression. The recent reports have provided evidence that early life exposure to BPA may increase susceptibility to hormonal carcinogenesis in the prostate gland, possibly by developmentally reprogramming carcinogenic risk Ho et al.
Knudsen et al. Subsequent in vivo analyses of the impact of BPA on human prostate tumor growth and recurrence were performed using a mouse xenograft of human cells containing the AR-TA mutation Wetherill et al. At low doses that fall within the reported ranges of human exposure, prostate tumor size increased in response to BPA administration when compared with placebo control and mice in the BPA cohort demonstrated an earlier rise in PSA biochemical failure.
These findings indicating that BPA significantly shortened the time to therapeutic relapse. These outcomes underscore the need for further study of the effects of BPA on tumor progression and therapeutic efficacy.
Persistent organic pollutants, such as PCBs, are fat soluble chemicals that bioaccumulate in the human body. Many have estrogenic or anti-androgenic activity and as such, may perturb male reproductive activity. A recent analysis of adipose tissue concentrations of PCBs in Swedish men with and without prostate cancer revealed a significant association between PCB levels in the higher quandrants and prostate cancer odds ratio with the most marked associations for PCB and trans-chlordane Hardell et al.
A more extensive epidemiologic study of capacitor manufacturing plant workers highly exposed to PCBs revealed a strong exposure—response relationship for prostate cancer mortality Prince et al.
This supports previous findings of correlations between PCB and and prostate cancer risk in electric utility workers Charles et al. While estrogenic activity of these compounds is a suspected mode of action, there is also evidence that PCBs inhibit estrogen sulfotransferase activity in the liver and effectively increase bioavailable estrogen in the body Kester et al.
Recently, Aroclor, a mixture of 60 PCB pollutants, was tested on rat prostate cells in vitro and shown to disrupt gap junctions, expression of connexin 32 and 43 and increase double-stranded DNA breaks suggesting that PCBs may be able to transform prostate cells leading to carcinogenesis Cillo et al. Further investigation using animal models is warranted for PCBs and prostate cancer risk. There are a few recent reports that UV light filters that are used to protect against the sun have estrogenic activity Schlumpf et al.
While little if any work has been done with regard to these UV filters and human prostate cancer, a few recent reports indicate that developmental exposure to the compounds can alter prostate gland development and estrogen target gene expression in the rat Schlumpf et al. This raises the possibility that the fetal prostate may be affected following maternal use of these compounds. Cadmium is known to ligand to ERs and function as an estrogenic mimic. Nonetheless, there are intriguing reports in the literature which show that cadmium has proliferative action with human prostate cells in vitro through an ER-dependent mechanism and that this exposure is associated with acquisition of androgen independence Benbrahim-Tallaa et al.
Furthermore, prostatic tumors have been shown to be experimentally induced by oral exposure to cadmium Waalkes Since cadmium bioaccumulates in the body, further epidemiologic analysis of cadmium and prostate cancer risk is warranted, particularly in men with occupational exposures. Exposure to arsenic has long been associated with a number of diseases including cancers Chen et al. Importantly, it has been documented that arsenic may mediate some of these effects through endocrine disruption, specifically through interaction with ERs and activation of estrogen-regulated genes Davey et al.
In this context, there is a recent report that arsenic can induce malignant transformation of prostate epithelial cells in vitro and drive them toward an androgen-independent state Benbrahim-Tallaa et al. Interestingly, this was shown to be mediated through Ras-MAPK pathways and it is possible that membrane ERs may be involved in this process. Epidemiologic studies have shown an association between arsenic exposure and prostate cancer mortality in Taiwan Chen et al.
Thus, it is possible that endocrine disruption by arsenic can contribute to prostate cancer risk. While there are no known environmental androgens, EDs can also function through anti-androgenic pathways. Since prostate cancer is an androgen-dependent disease, we will briefly examine the known effects of some of these agents on the prostate gland. Vinclozolin is a fungicide that is used as a pesticide on crops. Since vinclozolin effects are driven through AR antagonism, it is not surprising that there are no reported associations between this compound and prostate cancer, an androgen-dependent disease.
Exposure of rats to vinclozolin during development results in reduced prostate gland growth and size which would be expected for an anti-androgen Yu et al. Of interest, however, are recent studies with maternal i. This may be particularly significant in light of recent evidence that chronic inflammation may play a role in prostate cancer initiation Nelson et al.
In addition to AR antagonistic effects Gray et al. There is increasing evidence both from epidemiology studies and animal models that specific endocrine-disrupting compounds may influence the development or progression of prostate cancer.
In large part, these effects appear to be linked to interference with estrogen signaling, either through interacting with ERs or by influencing steroid metabolism and altering estrogen levels within the body.
In humans, epidemiologic evidence links specific pesticides, PCBs, and inorganic arsenic exposures to elevated prostate cancer risk. Studies in animal models also show augmentation of prostate carcinogenesis with several other environmental estrogenic compounds including cadmium, UV filters, and BPA. Importantly, there appears to be heightened sensitivity of the prostate to these EDs during the critical developmental windows including in utero and neonatal time points as well as during puberty.
Thus, infants and children may be considered a highly susceptible population for ED exposures and increased risk of prostate cancers with aging. There are several key questions that must be addressed in the future studies in order to best appreciate and understand the risks of prostate disease as they relate to endocrine-disrupting chemicals.
What specific ED chemicals can influence the prostate gland and increase prostate cancer risk or progression? Are there epigenetic pathways that mediate developmental exposures to EDs and prostate disease with aging? Does ED exposure influence prostate cancer susceptibility in subpopulations of men? Is the in utero developing human prostate sensitive to ED chemicals and do they influence prostate cancer risk in the aging male?
What are the most appropriate life stages for examining ED and prostate cancer risk? Focused research on these and other specific questions is required in order to adequately evaluate the human risk for prostate disease from the growing accumulation of EDs in the environment.
Insight into molecular mechanisms may help to provide biomarkers for prostate disease risk from ED exposure as well as to provide opportunities for therapeutic intervention. The authors declare that there is no conflict of interest that would prejudice the impartiality of this scientific work. Introduction Prostate cancer is the most common solid cancer in males and is the second leading cause of cancer deaths in American men Jemal et al.
Evidence and mechanisms Farming and pesticides Regarding links between prostate cancer and environmental factors in humans outside of diet , the most compelling data come from the established occupational hazard of farming and increased prostate cancer rates Morrison et al. Environmental estrogens In men, chronically elevated estrogens have been associated with increased risk of prostate cancer Modugno et al.
Diethylstilbestrol DES DES exposure is considered an important model of endocrine disruption and provides proof of principle for exogenous estrogenic agents as disruptors of multiple endorgans. Ultraviolet UV filters There are a few recent reports that UV light filters that are used to protect against the sun have estrogenic activity Schlumpf et al. Cadmium Cadmium is known to ligand to ERs and function as an estrogenic mimic.
Arsenic Exposure to arsenic has long been associated with a number of diseases including cancers Chen et al. Anti-androgens While there are no known environmental androgens, EDs can also function through anti-androgenic pathways. Vinclozolin Vinclozolin is a fungicide that is used as a pesticide on crops. Summary and key questions There is increasing evidence both from epidemiology studies and animal models that specific endocrine-disrupting compounds may influence the development or progression of prostate cancer.
What are their modes of action? Is there an additive or synergistic effect from ED mixtures and prostate cancer risk or growth? Is there a transgenerational risk for prostate cancer as a function of ED exposures? Can we establish molecular markers for ED exposures as they relate to prostate disease risk? Declaration of interest The authors declare that there is no conflict of interest that would prejudice the impartiality of this scientific work.
Resources for News Media. Asbestos is what we call a group of fibrous minerals, found in nature, that are resistant to heat and corrosion. To reduce your risk, limit your exposure to UV rays—both from the sun and indoor tanning—and wear sunscreen and protective clothing when outdoors. Adjusting to Cancer. Cancer Screening Overview. Childhood Cancers Research. Department of Health and Human Services HHS , and the International Agency for Research on Cancer IARC , the cancer agency of the World Health Organization—have developed lists of substances that, based on the available scientific evidence, are known or are reasonably anticipated to be human carcinogens.
Environmental toxins prostate cancer. CONTACT INFORMATION
The Centers for Disease Control and Prevention recommends that and year-old boys and girls receive two doses of the HPV vaccine six months apart, and that young men and women ages 15 to 26 receive three doses. Chronic infection with hepatitis B or hepatitis C virus is the most common risk factor for liver cancer. Both viruses are spread by sharing contaminated needles, unprotected sex and childbirth.
Also, the Epstein-Barr virus, which causes mononucleosis, is linked to some types of lymphoma. Currently, there are no vaccines for hepatitis C or Epstein-Barr, but there is a vaccine for hepatitis B.
Ionizing radiation is thought to cause about 1 percent of all cancers. When cancer treatments increase your risk of developing another cancer later in life, the decision-making process often involves weighing the risks against the benefits, says Glynis Vashi, MD, Intake Physician and Chief of Medicine at our hospital near Chicago. As medicine continues to evolve, scientists may discover more environmental substances that we should avoid, or at least limit in use.
Today, some possible but unproven risk factors include fluoride in water, radiation from power lines and electrical devices, chemicals in certain hair dyes and cosmetics, lead, the mineral talc in talcum powder, diesel exhaust and the chemical BPA in some plastics.
Perre says. The significance of environmental risk factors is underscored in cancer rate disparities throughout the world and how those rates fluctuate when people move from place to place. For example, people who live in Asia tend to have low rates of prostate and breast cancer and high rates of stomach cancer, but when they emigrate to the United States—where prostate and breast cancers are prevalent—their prostate and breast cancer rates rise over time. For example, one man may smoke for 30 years and never develop lung cancer, while another who only smoked in college may develop the disease years later.
Vashi says. That is when you realize that there is something at play beyond the environment. Understanding the relationship between the environment and genetics is vital to lowering your cancer risk, Dr. At the end of the day, you have the power to reduce potential exposures to substances in the environment, Dr. Hoag says. Call us anytime. Outpatient Care Centers. Becoming a Patient. Menu Search. How we treat cancer. Our locations. Becoming a patient.
For physicians. Call us anytime What are environmental risk factors, and how can I avoid them? February 22, by CTCA. Ultraviolet radiation Ultraviolet UV rays from the sun, sunlamps or tanning beds may damage cell DNA and lead to melanoma or other forms of skin cancer. Asbestos Asbestos occurs in rock and soil, and is often found in building construction materials for insulation. Viruses Certain viruses are linked to several types of cancer.
Ionizing radiation Ionizing radiation is thought to cause about 1 percent of all cancers. Related Articles. Study: Dr. Google a key consultant for majority of cancer patients Survey finds that majority of cancer patients of all generations increasingly rely on the internet to gather information after a cancer diagnosis. Damaged DNA can lead to changes in our cells, which then leads to cancer. Some of these substances can be avoided easily. When environmental toxins are in our water, air, or the materials used to perform our jobs, they are much more difficult to avoid.
Asbestos is what we call a group of fibrous minerals, found in nature, that are resistant to heat and corrosion. The naturally occurring substance has been used in commercial products such as insulation, fireproofing material, and indoor construction materials. We are all exposed to low levels of asbestos in the air. These low level exposures rarely cause any problems. Repeated exposures over time has a much more harmful effect. Exposure happens when these materials are installed, and when they are disturbed after installation.
When disturbed, the fibers become airborne, they are inhaled and become trapped in the lungs. The accumulation can affect breathing and lead to cancer and other health problems. Also significant statistics were noted for kidney cancer, cancer of the eye, and non-malignant respiratory disease in this study.
You can read the study here. NIH National Cancer Institute says, Formaldehyde is a colorless, strong-smelling, flammable chemical that is produced industrially and used in building materials such as particleboard, plywood, and other pressed-wood products. Since the s, the National Cancer Institute NCI , a component of the National Institutes of Health NIH , has conducted studies to determine whether there is an association between occupational exposure to formaldehyde and an increase in the risk of cancer.
Endocrine disruptors and prostate cancer risk in: Endocrine-Related Cancer Volume 15 Issue 3 ()
In fiction, arsenic is best known as a poison; the metal is so notorious that it's been called the king of poisons. In fact, arsenic has been used by so many members of royal households that it's also been called the poison of kings. But arsenic is much more than a murderer's tool. In the past, it was used to treat a variety of illnesses, ranging from sleeping sickness and syphilis to psoriasis and leukemia. It was also used in many pesticides.
And even though medicinal and agricultural uses of arsenic have been largely abandoned, the metal still has a variety of industrial uses; the list includes wood preservatives, lead-acid batteries, automotive body solder, and semiconductor applications.
Arsenic is also widely distributed in the environment. Natural deposits are present in soil and rocks; high levels are found near industrial sites and hazardous waste sites. And arsenic can run off from soil and industrial waste to enter drinking water, making the infamous metal a concern for everyone.
Arsenic makes a good murder weapon because a single high dose can poison the metabolism, causing intestinal bleeding, heart, liver, and kidney failure, coma, and death. Long-term exposure to lower levels can produce skin discoloration and may lead to blood vessel disease, nerve damage, and abdominal pain. And a study found that even low levels of arsenic in America's drinking water are linked to an increased risk of diabetes.
More than years ago, skin cancer was recognized as a complication of arsenic toxicity. Since then, scientists have learned that arsenic exposure also increases the risk of lung, kidney, bladder, and liver cancers. When people are exposed to excessive amounts of arsenic, high levels of the metal enter the urine.
That may explain the link between arsenic and cancers of the kidney and bladder. But can arsenic also increase the risk of prostate cancer? When researchers from the National Cancer Institute reviewed the evidence in , they concluded that the answer is yes. They based their finding on two lines of evidence. Laboratory experiments show that arsenic can trigger the malignant transformation of human prostate cells.
Moreover, only low levels of arsenic are needed to convert cells from normal to cancerous. And when these human prostate cancer cells are taken from laboratory culture dishes and implanted into mice, they grow into aggressive tumors that produce excess amounts of prostate-specific antigen PSA.
In short order, these tumors also escape the influence of male hormones androgens , mimicking the behavior of the most aggressive androgen-independent human prostate cancers. Human population studies bolster the case. Most of the evidence comes from Taiwan, where drinking water from some local artesian wells contains high levels of arsenic. Researchers were able to compare men with different arsenic exposures but otherwise similar lifestyles, living conditions, diets, and socioeconomic status.
They found that men with the highest arsenic exposures were nearly six times more likely to die from prostate cancer than men with less intense exposures. Drinking water in the U. Erectile dysfunction ED and prostate cancer are entirely distinct problems, but researchers in Taiwan have linked both to arsenic. In all, the risk of severe ED was 7. Arsenic was also linked to reduced levels of testosterone, but arsenic remained an ED risk factor even after the results were adjusted for testosterone.
The link also persisted after researchers accounted for traditional ED risk factors such as diabetes, hypertension, smoking, and cardiovascular disease. For arsenic, that level is 0. Recognizing that perfection is rarely attainable, the EPA and the World Health Organization set 10 parts per billion as the safe upper limit for arsenic in drinking water; that's roughly equivalent to a few drops of ink in an Olympic-sized swimming pool.
All community water systems are required to meet or exceed this goal. If your water comes from a private source, your local water department can refer you to a certified lab for testing. Prostate cancer is a puzzle, and arsenic is only a small part of the solution. Apart from industrial exposures and accidents, it's not a major concern for most American men.
But when it comes to health, every drop of safety counts. Disclaimer: As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.
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