Quantitative estimation of essential/toxic elemental levels in the serum of esophagus cancer patients in relation to controls

Environmental Science and Pollution Research - Esophageal cancer is a very deadly disease ranking 8th most common cancer in terms of incidence and the 6th highest in terms of mortality both in the...     

Radon versus other lung cancer risk factors: How accurate are the attribution estimates?

This notebook paper provides a brief overview of attribution estimates for some key lung cancer risk factors, focusing on indoor radon gas exposure in the U.S., UK, and Canada. Tobacco smoking represents the primary cause of lung cancer worldwide. Radon is regarded as the second leading lung cancer risk factor in the U.S. and Canada. It can be observed, however, that the reported estimates appear not to add up to the maximum cumulative attribution of 100%.

Implications: Limitations and uncertainties associated with published epidemiological studies and the observed lack of consistency in lung cancer attribution estimates for radon and other non-smoking lung cancer risk factors should be taken into consideration by policy makers in setting population health protection priorities.     

Health risks from arsenic-contaminated soil in Flin Flon–Creighton,Canada: Integrating geostatistical simulation and dose–response model

Elevated concentrations of arsenic were detected in surface soils adjacent to a smelting complex in northern Canada. We evaluated the cancer risks caused by exposure to arsenic in two communities through combining geostatistical simulation with demographic data and dose–response models in a framework. Distribution of arsenic was first estimated using geostatistical circulant-embedding simulation method. We then evaluated the exposures from inadvertent ingestion, inhalation and dermal contact. Risks of skin caner and three internal cancers were estimated at both grid scale and census-unit scale using parametric dose–response models. Results indicated that local residents could face non-negligible cancer risks (skin cancer and liver cancer mainly). Uncertainties of risk estimates were discussed from the aspects of arsenic concentrations, exposed population and dose–response model. Reducing uncertainties would require additional soil sampling, epidemic records as well as complementary studies on land use, demographic variation, outdoor activities and bioavailability of arsenic.     

Evaluation of risks from urban air pollutants in the southeast Chicago area

Region V of the U.S. Environmental Protection Agency has conducted a comprehensive study of cancer risks from urban exposure to air pollutants in the Southeast Chicago area. This study estimated emissions of a list of 30 air carcinogens from a broad range of nontraditional, as well as traditional, source types. Using dispersion modeling and applying the appropriate unit risk factors and population data, this study estimated the risks at each receptor location and the total number of cancer cases attributable to air pollution in the area. This analysis estimated that current concentrations would cause 77 cases of cancer over the next 70 years, an average risk of 2.0 X 10(-4). Contributions from different source types and different pollutants were estimated. The total contribution from nontraditional source types was less than 0.3 percent. Although these estimates are highly uncertain, the study does suggest the nature and general magnitude of cancer risks from air pollution in the urban area studied.     

Odor Control In Los Angeles County

Abstract

Concentrations of 38 gas-phase organic air toxics were measured over a 2-yr period at four different sites in and around Pittsburgh, PA, to investigate spatial variations in health risks from chronic exposure. The sites were chosen to represent different exposure regimes: a downtown site with substantial mobile source emissions; two residential sites adjacent to one of the most heavily industrialized zones in Pittsburgh; and a regional background site. Lifetime cancer risks and non-cancer hazard quotients were estimated using a traditional and interactive risk models. Although study average concentrations of specific air toxics varied by as a much as a factor of 26 between the sites, the additive cancer risks of the gas-phase organic air toxics varied by less than a factor of 2, ranging from 6.1 × 10^-5 to 9.5 × 10^-5. The modest variation in risks reflects the fact that two regionally distributed toxics, formalde-hyde and carbon tetrachloride (CCl₄), contributed more than half of the cancer risk at all four sites. Benzene contributed substantial cancer risks at all sites, whereas trichloroethene and 1,4-dichlorobenzene only contributed substantial cancer risks at the downtown site. Only acrolein posed a non-cancer risk. Diesel particulate matter is estimated to pose a much greater cancer risk in Pittsburgh than other classes of air toxics including gas-phase organic, metals, polycyclic aromatic hydrocarbons, and coke oven emissions. Health risks of air toxics in Pittsburgh are comparable with those in other urban areas in the United States.     

Farmland transfer and esophageal cancer incidence rate: mediation of pollution-related agricultural input intensity

Environmental Science and Pollution Research - Cancer is a growing global health threat. Examining the determinants of cancer incidence can benefit for cancer treatment and prevention. Farmland...     

Health Effects of Waste Incineration: A Review of Epidemiologic Studies

ABSTRACT

There is an increasing trend toward using incineration to solve the problem of waste management; thus, there are concerns about the potential health impact of waste incineration. A critical review of epidemiologic studies will enhance understanding of the potential health effects of waste incineration and will provide important information regarding what needs to be investigated further. This study reviews the epidemiologic research on the potential health impact of waste incineration. Previous studies are discussed and presented according to their study population, incinerator workers or community residents, and health end points. Several studies showed significant associations between waste incineration and lower male-to-female ratio, twinning, lung cancer, laryngeal cancer, ischemic heart disease, urinary mutagens and pro-mutagens, or blood levels of certain organic compounds and heavy metals. Other studies found no significant effects on respiratory symptoms, pulmonary function,twinning, cleft lip and palate, lung cancer, laryngeal cancer,or esophageal cancer. In conclusion, these epidemiologic studies consistently observed higher body levels of some organic chemicals and heavy metals, and no effects on respiratory symptoms or pulmonary function. The findings for cancer and reproductive outcomes were inconsistent. More hypothesis-testing epidemiologic studies are needed to investigate the potential health effects of waste incineration on incinerator workers and community residents.     

Health effects of waste incineration: a review of epidemiologic studies

There is an increasing trend toward using incineration to solve the problem of waste management; thus, there are concerns about the potential health impact of waste incineration. A critical review of epidemiologic studies will enhance understanding of the potential health effects of waste incineration and will provide important information regarding what needs to be investigated further. This study reviews the epidemiologic research on the potential health impact of waste incineration. Previous studies are discussed and presented according to their study population, incinerator workers or community residents, and health end points. Several studies showed significant associations between waste incineration and lower male-to-female ratio, twinning, lung cancer, laryngeal cancer, ischemic heart disease, urinary mutagens and promutagens, or blood levels of certain organic compounds and heavy metals. Other studies found no significant effects on respiratory symptoms, pulmonary function, twinning, cleft lip and palate, lung cancer, laryngeal cancer, or esophageal cancer. In conclusion, these epidemiologic studies consistently observed higher body levels of some organic chemicals and heavy metals, and no effects on respiratory symptoms or pulmonary function. The findings for cancer and reproductive outcomes were inconsistent. More hypothesis-testing epidemiologic studies are needed to investigate the potential health effects of waste incineration on incinerator workers and community residents.     

Evaluation of Risks from Urban Air Pollutants in the Southeast Chicago Area

Region V of the U.S. Environmental Protection Agency has conducted a comprehensive study of cancer risks from urban exposure to air pollutants in the Southeast Chicago area. This study estimated emissions of a list of 30 air carcinogens from a broad range of nontraditional, as well as traditional, source types. Using dispersion modeling and applying the appropriate unit risk factors and population data, this study estimated the risks at each receptor location and the total number of cancer cases attributable to air pollution in the area.

This analysis estimated that current concentrations would cause 77 cases of cancer over the next 70 years, an average risk of 2.0 × 10^?4. Contributions from different source types and different pollutants were estimated. The total contribution from nontraditional source types was less than 0.3 percent. Although these estimates are highly uncertain, the study does suggest the nature and general magnitude of cancer risks from air pollution in the urban area studied.     

Berberine-loaded liquid crystalline nanoparticles inhibit non-small cell lung cancer proliferation and migration in vitro

Environmental Science and Pollution Research - Non-small cell lung cancer (NSCLC) is reported to have a high incidence rate and is one of the most prevalent types of cancer contributing towards 85%...     

Low-level arsenic exposure is associated with bladder cancer risk and cigarette smoking: a case–control study among men in Tunisia

Although exposure to high levels of arsenic is associated with excess bladder cancer risk, lower exposures generally are not. This study represents the first biomonitoring of arsenic exposure in Tunisia and focuses on a possible association with bladder cancer risk. In this context, 124 male bladder cancer cases and 220 controls were recruited and blood samples were analyzed to determine the concentration of As. The study subjects were stratified into median groups based on concentrations of arsenic in their blood. Blood arsenic (B-As) was significantly two to threefold higher in bladder cancer cases than in controls (p?<?0.05). The arsenic concentrations were significantly higher among both smokers and workers in construction. However, neither drinking water nor seafood was found to be incriminated as exposure sources. The adjusted risk ratios for B-As concentration categories 0.1–0.67 and ≥0.67 μg/L were 0.18 (95% CI?=?0.014–2.95) and 2.44 (95% CI?=?1.11–5.35), respectively. Arsenic levels were not found to be associated with tumor grade or stage. The considerable risk in the category of highest cumulative exposure argues for an association between bladder cancer risk and low-level arsenic exposure. Future investigations with larger samples and using techniques that allow the distinction of the different arsenic species should better elucidate this association. Furthermore, the modulation of arsenic level according to the histological grade may be of potential to be used as a diagnostic marker of the disease process and its possible relationship etiologically.     

Environmental exposure to PCBs and cancer incidence in eastern Slovakia

In a population-based cross-sectional study, we compared serum levels of 15 polychlorinated biphenyl (PCB) congeners and three organochlorine pesticides in residents of two districts in eastern Slovakia, one with extensive environmental contamination from a former PCB production site (Michalovce) and the other matched on geography but with low (background) levels (Svidnik). The age-adjusted geometric means for sum of 15 measured PCB congeners were statistically significantly higher in subjects from the Michalovce district for both sexes: 3327.6 versus 1331.4 ng/g of lipid in males, 2751.8 versus 992.2 ng/g of lipid in females. Levels of DDE and DDT were also significantly higher, although the absolute differences were less pronounced. There was no substantial difference in HCB levels between the districts. We also conducted an ecologic study to compare cancer incidence occurring in these same two districts from 1985 through 1994. We calculated standardized incidence ratios (SIRs) and 95% confidence intervals for each district using indirect standardization and rates from eastern Slovakia. Among males from Michalovce (exposed), but not Svidnik (unexposed), there was an excess of cancer of the tongue (SIR=1.46; 1.06-1.96), stomach (SIR=1.15; 1.00-1.32), lung (SIR=1.14; 1.04-1.24), testis (SIR=1.40; 0.97-1.97), and kidney (SIR=1.23; 0.98-1.52), and lower than expected incidence of prostate cancer (SIR=0.83; 0.69-0.97); in contrast, there was an excess of peritoneal (SIR=3.05; 1.11-6.63) and laryngeal cancer (SIR=1.43; 0.99-1.98) in Svidnik not observed Michalovce. Among females from Michalovce, but not Svidnik, there was an excess of cancer of the lip (SIR=2.54; 1.53-3.96), stomach (SIR=1.22; 1.02-1.44), and lung (SIR=1.17; 0.94-1.45); in contrast, there was an excess of kidney (SIR=1.61; 1.03-2.40) and thyroid (SIR=1.97; 1.12-3.20) cancer in Svidnik not observed in Michalovce. Taken together, these results raise the possibility that high environmental exposure to organochlorines in the Michalovce district may be associated with higher rates of certain cancers, particularly stomach and lung cancer.     

Screening-level Assessment of Airborne Carcinogen Risks from Uncontrolled Waste Sites

This report presents screening-level estimates of the general level of cancer risks arising from air emission from uncontrolled waste sites. Twenty-five National Priorities List sites were chosen randomly and airborne cancer risks estimated for each site in terms of risk to the maximally exposed individual (MEI risk), average individual risk (AEI risk), and population incidence. The estimates were developed using the EPA Human Exposure Model using assumptions on the rate and toxicity of site emissions.

MEIrisks ranged from 4 × 10^-9 to 1 × 10^-6 with an average of about 5 × 10^-7. AEI risks for individuals residing within four miles of the sites average about 10^-8, declining significantly for individuals residing at longer distances. Population incidence was low at all sites ranging from 2 × 10^-4 to 1 × 10^-2 cancer cases expected within 60 miles of the sites. Due to the uncertainties in this type of analysis and the underlying study assumptions, these results must be viewed with caution. Nonetheless, some preliminary conclusions can be drawn from the analysis, principally that airborne cancer risks from uncontrolled waste sites are likely to be small in most cases, with the greatest concern being maximally exposed individuals rather than the number of cancer cases expected in the exposed population.     

Quantitative cancer risk assessment and local mortality burden for ambient air pollution in an eastern Mediterranean City

Health risks posed by ambient air pollutants to the urban Lebanese population have not been well characterized. The aim of this study is to assess cancer risk and mortality burden of non-methane hydrocarbons (NMHCs) and particulates (PM) based on two field-sampling campaigns conducted during summer and winter seasons in Beirut. Seventy NMHCs were analyzed by TD-GC-FID. PM_2.5 elemental carbon (EC) components were examined using a Lab OC-EC aerosol Analyzer, and polycyclic aromatic hydrocarbons were analyzed by GC-MS. The US EPA fraction-based approach was used to assess non-cancer hazard and cancer risk for the hydrocarbon mixture, and the UK Committee on Medical Effects of Air Pollutants (COMEAP) guidelines were followed to determine the PM_2.5 attributable mortality burden. The average cumulative cancer risk exceeded the US EPA acceptable level (10⁻⁶) by 40-fold in the summer and 30-fold in the winter. Benzene was found to be the highest contributor to cancer risk (39–43%), followed by 1,3-butadiene (25–29%), both originating from traffic gasoline evaporation and combustion. The EC attributable average mortality fraction was 7.8–10%, while the average attributable number of deaths (AD) and years of life lost (YLL) were found to be 257–327 and 3086–3923, respectively. Our findings provide a baseline for future air monitoring programs, and for interventions aiming at reducing cancer risk in this population.

     

Evaluation of the mortality experience of workers exposed to the chlorinated dioxins

Mortality patterns were analyzed for the time period 1940 through 1979 of 2,189 men with potential occupational exposure to chlorinated dibenzo-p-dioxins. Special attention was directed toward 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) and deaths due to soft-tissue sarcoma, non-Hodgkins lymphoma, Hodgkins disease, liver cancer, stomach cancer, and nasal or nasopharyngeal cancer. With United States white males as the comparison population for this employee cohort, the stadardized mortality ratio for all causes of death was 91 and for total malignant neoplasms, 96. Among the malignancy categories of particular interest, none demonstrated a significant deviation from expected. Nor were any significant trends noted for any specific cause of death category when analyzed by estimated cumulative exposure.     

Breast cancer and persistent organic pollutants (excluding DDT): a systematic literature review

Persistent organic pollutants (POPs) are a group of heterogeneous compounds of both natural and anthropogenic origin with highly persistent and bioaccumulative properties. They cause a range of adverse effects to human health and the environment around the world. There is growing concern that POPs may increase breast cancer risk due to their xenoestrogenic properties. The aim of this systematic literature review is to summarize and integrate the risks of breast cancer following environmental exposure to POPs (other than DDT) from primary epidemiological studies published between 2006 and 2015. After searching various databases, 14 case-control studies and one cohort study were included. Evidence of an association between increased breast cancer risk and environmental exposure to these chemicals is inconsistent and inadequate to conclude with certainty. However, most of the studies have examined exposure to the pollutants after diagnosis of breast cancer, overlooking exposure during critical windows of vulnerability. They have also largely focused on individual chemicals but ignored the combined effects of different chemicals. Therefore, major data gaps remain in examining exposure during critical windows of vulnerability and assessing combined effects of multiple chemicals. Development of better exposure assessment methods addressing these gaps is required for future research.     

Dioxin exposure and public health in Chapaevsk, Russia

One of the largest environmental polluters in Chapaevsk (Samara Region, Russia) is the Middle Volga chemical plant. From 1967 to 1987, it produced hexachlorocyclohexane (lindane) and its derivatives. Currently, it produces crop protection chemicals (liquid chlorine acids, methyl chloroform, vinyl chloride, and some other chemicals). Dioxins were detected in air (0.116 pg/m3), in soil (8.9-298 ng/kg), in the town's drinking water (28.4-74.1 pg/liter), and in the cow's milk (the content of 2,3,7,8-TCDD was 17.32 pg TEQ/g fat). The mean content of dioxins in seven pooled samples of human milk (40 individual trials) was 42.26 pg TEQ/g fat, in four female workers' blood samples -412.4 pg TEQ/g fat, in six residents blood samples (those who lived 1-3 km from the chemical plant) -75.2 pg TEQ/g fat, in four residents' blood samples (5-8 km from the plant) -24.5 pg TEQ/g fat. To assess cancer risk and reproductive health status, official medical statistical information was used. In general, the male cancer mortality observed rate in Chapaevsk is higher than expected. The SMR is higher for lung cancer 3.1(C.I. 2.6-3.8), urinary organs 2.6(C.I. 1.7-3.6). Chapaevsk women have a higher risk overall due to breast cancer 2.1(C.I. 1.6-2.7) and cervix cancer 1.8(C.I. 1.0-3.1). The incidence rates were higher for lung cancer in males and for female breast cancer in all age groups compared to Russia and Samara Region in 1998. Significant disruptions in reproductive function were detected. The mean frequency of spontaneous abortions in the last seven years was statistically higher 24.4% in Chapaevsk (compared to other of the towns region). The average rate of premature labor was 45.7 per 1000 women in Chapaevsk that is significantly higher than in most Samara Region towns. The frequency of newborns with low birth weight was 7.4%. In Russia and in most of the Samara Region towns, this rate is lower (6.2-5.1%) but not statistically different. For the determination of congenital morphogenetic conditions (CMGC), 369 children born between 1990 and 1995 were examined. The average number of CMGC per child was significantly higher, 4.5 for boys and 4.4 for girls. The first results indicated serious disruptions associated with high dioxin levels in human milk and blood in Chapaevsk. We suggest that Chapaevsk is an incredibly interesting site for further environmental-epidemiological research to assess the impact of dioxins on human health.     

PCB exposure and potential future cancer incidence in Slovak children: an assessment from molecular finger printing by Ingenuity Pathway Analysis (IPA®) derived from experimental and epidemiological investigations

The risk of cancer due to PCB exposure in humans is highly debated. In eastern Slovakia, high exposure of the population to organochlorines (especially PCBs) was associated with various disease and disorder pathways, viz., endocrine disruption, metabolic disorder & diabetes, and cancer, thereby disturbing several cellular processes, including protein synthesis, stress response, and apoptosis. We have evaluated a Slovak cohort (45-month children, at lower and higher levels of PCB exposure from the environment) for disease and disorder development to develop early disease cancer biomarkers that could shed new light on possible mechanisms for the genesis of cancers under such chemical exposures, and identify potential avenues for prevention.

Microarray studies of global gene expression were conducted from the 45-month-old children on the Affymetrix platform followed by Ingenuity Pathway Analysis (IPA®) to associate the affected genes with their mechanistic pathways. High-throughput qRT-PCR TaqMan low-density array (TLDA) was performed to further validate the selected genes on the whole blood cells of the most highly exposed children from the study cohort (n = 71).

TP53, MYC, BCL2, and LRP12 differential gene expressions suggested strong relationships between potential future tumor promotion and PCB exposure in Slovak children. The IPA analysis further detected the most important signaling pathways, including molecular mechanism of cancers, prostate cancer signaling, ovarian cancer signaling, P53 signaling, oncostatin M signaling, and their respective functions (viz., prostate cancer, breast cancer, progression of tumor, growth of tumor, and non-Hodgkin’s disease). The results suggest that PCB exposures, even at the early age of these children, may have lifelong consequences for the future development of chronic diseases.

     

Cadmium as a possible cause of bladder cancer: a review of accumulated evidence

Bladder cancer is a significant disease, the rates of which have increased over the few last years. However, its etiology remains as yet undefined. Cadmium, a widespread environmental carcinogen that has received considerable interest, presents evidence as a possible cause of bladder cancer. A literature review was conducted from the years 1984–2013 to study the accumulated evidence for cadmium as a possible cause of bladder cancer, including routes of cadmium exposure, accumulation, toxicity, carcinogenicity, and evidence from epidemiological and experimental studies. Special reference is devoted to cadmium nephrotoxicity, which illustrates how cadmium exerts its effects on the transitional epithelium of the urinary tract. Mechanisms of carcinogenesis are discussed. The effects of cadmium on gene expression in urothelial cells exposed to cadmium are also addressed. Despite different methodologies, several epidemiologic and nephrotoxicity studies of cadmium indicate that occupational exposure to cadmium is associated with increased risk of bladder cancer and provide additional evidence that cadmium is a potential toxic element in urothelial cells. In vitro studies provide further evidence that cadmium is involved in urothelial carcinogenesis. Animal studies encounter several problems such as morphology differences between species. Among the complex mechanisms of cadmium carcinogenesis, gene expression deregulation is the subject of recent studies on bladder cadmium-induced carcinogenesis. Further research, however, will be required to promise a better understanding of the mechanisms underlying cadmium carcinogenesis and to establish the precise role of cadmium in this important malignancy.     

On Air Pollution,Environmental Tobacco Smoke,Radon, and Lung Cancer

The health of populations in industrialised societies has been affected for many years by ambient air pollutants presenting a threat of chronic bronchitis and lung cancer. In the 1980s Indoor pollutants received much needed investigation to assess their hazards to health. Exposure to environmental tobacco smoke and radon is now the subject of much research and concern. This review attempts to put some perspective on lung cancer that is attributable to lifetime exposure to airborne pollutants. The view is expressed that air pollution control authorities have played and are playing a major role in health improvement.