Environment and Prostate Cancer.
Introduction
Prostate cancer takes the lead as the most commonly diagnosed type of cancer disease among men in America and second globally (Donkena & Young, 2011, par.1). This disease has been linked to occupational and environmental risk factors to which when men get exposed to, they are likely to develop the disease, some of which include Agent Orange exposure, agricultural chemicals such as pesticides, ultra-violate radiations from the sun, tire and battery making trace minerals. Prostate cancer affects the prostate glands found in the male reproductive system and produces the seminal fluid that, in turn, nourishes and aids in the transportation of sperms (Ragin et al. 2012, par.3). This cancer grows slowly within the prostate gland during its onset but later on spreads quickly to other neighboring tissues once it grows outside the gland. The disease has a higher chance of treatment when detected early when it still is within the confinement of the prostate gland poses a serious treatment challenge after it spreads to other neighboring tissues. Environmental factors play a role in the high prevalence of prostate among men worldwide (Barry et al. 2012, par.2). Some of the environmental factors responsible for the high prevalence of prostate cancer among men include exposure to ultra-violate light and long period exposure to pesticides.
Ultra-violate rays.
Vitamin D is an essential element for the physiologic body activities and is obtained from sources such as naturally through the exposure of the body to sunlight, fortified vitamin D as a component of commonly used foodstuffs (Donkena & Young, 2011, par.9). Studies suggest that the natural pathway of vitamin D synthesis is never fully utilized due to the avoidance of the adverse consequences of long time exposure of the skin to sunlight. The most important of these effects is skin carcinogenesis, which poses a high risk of development of skin cancer hence making people limit the duration of exposure to sunlight. This consequently limits the quantity of vitamin D synthesized naturally in the body. The vitamin D synthesis pathway is responsible for the development and progression of cancers such as prostate cancer in men (Donkena & Young, 2011, par.12). Ultra-violate rays from the sun are a crucial catalyst of the vitamin D synthesis pathway in the skin where the skin cells synthesize 7-dihydro cholesterol, which then gets converted to vitamin D3 through the isomerization in the presence of ultra-violate radiation from sunlight. Uncontrolled farther photoreaction of vitamin D3 in the presence of UV light leads to the development of inactive metabolites. It is converted to calcidiol 25(OH)D3 in the liver by the enzyme in the mitochondrion sterol, 27-hydroxylase and then ultimately converted to the active vitamin D, calcitriol, 1,25-dihydroxy vitamin D3 by the enzyme 1α-hydroxylase found in the kidney and other tissues including the prostate (Donkena & Young, 2011, par.10). The intermediate form calcidiol 25(OH)D3 is used to determine the nutritional status of vitamin D in blood since it forms the predominant form present in the bloodstream and is additionally the form with the longer life span compared to calcitriol, 1,25-(OH)D3
The prostate cells have the capability of producing the active form of vitamin D3, as evidenced by the presence of 25(OH)D3, 1-α hydroxylase in the prostate cells. The activity of 1-α hydroxylase enzyme has been demonstrated in the cancerous cell lines of the prostate. The presence of 25(OH)D3 in high concentration in the prostatic cells
enhances the expression of 1-α hydroxylase, which then acts as anti-prostate cancer (Donkena & Young, 2011, par.11). The 25(OH)D3, therefore, can be used as an anti-prostate cancer agent. Antagonistically, 24-hydroxylase inactivates the 1,25(OH)D3, thereby inducing resistance to the antiproliferation effects of 1, 25(OH)2D3. Ultra-violate rays from the sun is a risk factor that predisposes men to prostate cancer by way of inducing metabolic changes in the prostatic cells by altering the formation of provitamin D3 and related metabolic enzyme and their expression in the genome coding system (Donkena & Young, 2011, par.13). Reduced expression of provitamin D3 (calcidiol) and hence its circulation that is occasioned by the reduction in the expression of 24-hydroxylase enzyme induces the proliferation of the cancerous prostatic cells leading to the development or the migration of cancer to the neighboring tissues around the prostate. On the contrary, elevated concentrations of the provitamin D3 and 24-hydroxylase in the prostatic cells hinder the proliferation of the cancerous prostatic cells, thereby inhibiting the development and movement of cancerous cells. Excess exposure to sunlight avails excess ultra-violate rays that then catalyzes the conversion of the provitamin D3 (calcidiol) into the active calcitriol, 1, 25(OH)D3 in the bloodstream (Donkena & Young, 2011, par.15). The reduced concentration of provitamin D3 in the bloodstream reduces its cancer inhibitory role ability hence predisposing one to the development of prostate cancer. Sunlight produces ultra-violate rays that catalyze the synthesis of vitamin D3 intermediate calcidiol and the active form of vitamin D calcitriol that both play inverse roles in the development and regulation of prostate cancer development.
Parallel studies on the effect of sunlight suggest that vitamin D displays anticancer activities, a phenomenon majorly associated with the vitamin D nuclear receptor VDR. The VDR functions by binding transcription factors within the nucleus upon which they inhibit the expression of the genes of the oncogenic cells, thereby preventing the development of cancer and its subsequent migration to other tissues (Donkena & Young, 2011, par.17). Sunlight as an environmental factor, thus plays a role in the development of prostate cancer among men through excessive exposure to it.
Exposure to pesticides
Pesticides constitute another risk factor for the development of prostate cancer among the men in the world over. This factor predisposes both the men who work in the agricultural fields hence rendered indirectly in contact with the herbicides and those who reside around the plantation fields where the pesticides are sprayed to protect crops from wanton destruction by pests (Barry et al. 2012. Par.1). Studies done by the University of South California indicated that men from the agricultural regions of California otherwise referred to as the Central Valley, faced a greater risk of developing prostate cancer due to exposure to pesticides. People get exposed to pesticides containing methyl bromide and organochlorines in the environment through inhalation and through the food people eat hence posing reasons.
Methyl bromide. Also referred to as bromomethane is an agricultural chemical that is used in the United States of America to fumigate soil in plantations for crops such as tomatoes and strawberries in a bid to control various pests (Barry et al. 2012. Par.3). Besides its use as a soil fumigant, it is also used as a post-harvest pesticide for most agricultural products. Additionally, methyl bromide is used to treat imported goods with the aim of preventing the spread of a foreign breed of pests in a country through imported agricultural goods. Other being a risk factor for prostate cancer, methyl bromide is a leading air pollutant that contributes to the depletion of the ozone layer hence causing the greenhouse effect. Its use was banned in the United States from 1993-2005, a phenomenon that has led to a decline in its supply in the country (Barry et al. 2012. Par.7). It was classified as a class 1 chemical hence profiling it in the group of highly toxic chemicals whose unauthorized use is punishable. Some of the toxicity consequences of its use include acute effects in the nervous system and the cardiovascular system that can potentially cause the death of those affected (Ragin et al. 2012, par.5). The chemical was named declared carcinogenic by the National Institute of Occupational Safety and Health (NIOSH). Its genotoxicity activity presents evidence of its carcinogenicity. Studies have found it capable of inducing DNA adducts through methylation of DNA bases, which then induces mutations of the nucleic acids (Barry et al. 2012. Par.11) The mutations then cause changes in the cell signaling pathways leads to the development of carcinomas in the prostate cells, therefore responsible for the high prevalence of prostate cancer among the men who get exposed to methyl bromide pesticides in the plantation fields and its surrounding.
Organochlorines consist of organic compounds with chlorine in their structures that have been modified to produce pesticides that are, in turn, used to kill pests hence helping to preserve produce and to protect crops from destruction (Gourounti & Andreas, 2020. Par.2). Organochlorine pesticides include DDT, dieldrin, aldrin, and lindane, among others. The most abundant nonpesticide organochlorine compound is the polychlorinated biphenyls (PCBs) and the dichlorodiphenyltrichloroethane (DDT) that were one on a wide use in the United States. These groups of pesticides also harbor carcinogenic characteristics hence making them potential risk factors for prostate cancer among men worldwide (Ragina, 2012, par.4). Exposure to the chemicals of this group of pesticides potentially causes prostate cancer to men hence contributing to the high prevalence of prostate cancer among men working in the large plantations where these pesticides are frequently sprayed to control pests in the large farms from destroying crops (Gourounti & Andreas, 2020. Par.4). Organochlorine compounds are stable hence resistant to decomposition via biochemical or physical processes, less soluble in water, and highly soluble in hydrocarbons. Humans get exposed to them through skin absorption, inhalation, and ingestion of food and water. It is capable of inducing hormonally related cancer such as breast cancer, testes cancer, and prostate cancer. The organochlorine compounds cause prostate cancer by disrupting the hormonal activities in the prostate glands that either leads to the overstimulation of prostatic cells to overreact hence function abnormally (Gourounti & Andreas, 2020. Par.3). Overstimulation or under-stimulation causes a change in the signaling pathways, which may, in turn, lead to mutations in the gene expression of cell functions, thereby causing uncontrolled cell proliferation leading to prostate cancer in men.
Conclusion
Environmental factors are responsible for the development and hence high prevalence of prostate cancer in the world over. Exposure to excess sunlight and pesticides present some of the environmental risk factors of prostate cancer among men. Sunlight, through the ultra-violate rays, catalyzes the synthesis of provitamin D3, an intermediate of vitamin D3 whose high concentration in the blood inhibits the development of prostate cancer. In contrast, suppression of its concentration, together with the 24-hydroxylase enzyme, poses the risk of the development of cancer. Exposure to pesticides equally induces cancer development in men by causing mutations in gene expression hence signaling the uncontrolled proliferation of the prostatic cells.
Works Cited
Gourounti, Kleanthi, and Lazaris Andreas. “Burden of Organochlorine Substances As a Risk Factor of Breast Cancer | Insight Medical Publishing.” Health Science Journals | High Impact Articles List, 2020, www.hsj.gr/medicine/burden-of-organochlorine-substances-as-a-risk-factor-of-breast-cancer.php?aid=3649.
Barry, Kathryn H., et al. “Methyl Bromide Exposure and Cancer Risk in the Agricultural Health Study.” PubMed Central (PMC), 2012, www.ncbi.nlm.nih.gov/pmc/articles/PMC3430844/.
Donkena, Krishna V., and Charles Y. Young. “Vitamin D, Sunlight, and Prostate Cancer Risk.” PubMed Central (PMC), 2011, www.ncbi.nlm.nih.gov/pmc/articles/PMC3170721/.
Ragin, Camille, et al. “Farming, Reported Pesticide Use, and Prostate Cancer.” PubMed Central (PMC), 2012, www.ncbi.nlm.nih.gov/pmc/articles/PMC3662981/.