Lung cancer and phosphates

In the United States, counties with phosphate mining or processing facilities frequently also have significantly elevated rates of mortality from lung cancer. To deduce this result, the locations of areas having high mortality rates from lung cancer have been compared with those containing phosphate deposits, mines, or processing plants. The results for both white and nonwhite populations show correlations which are improbable by pure chance. They should be examined on a site-by-site basis to establish whether ²²²Rn emissions from ²²⁶Ra are a significant factor in the elevated cancer mortality.     

A quantitative estimate of nonsmokers' lung cancer risk from passive smoking

This work presents a quantitative assessment of nonsmokers' risk of lung cancer from passive smoking. The estimates given should be viewed as preliminary and subject to change as improved research becomes available. It is estimated that U.S. nonsmokers are exposed to from 0 to 14 mg of tobacco tar per day, and that the typical nonsmoker is exposed to 1.4 mg per day. A phenomenological exposure-response relationship is derived, yielding 5 lung cancer deaths per year per 100,000 persons exposed, per mg daily tar exposure. This relationship yields lung cancer mortality rates and mortality ratios for a U.S. cohort which are consistent to within 5% with the results of both of the large prospective epidemiological studies of passive smoking and lung cancer in the United States and Japan. Aggregate exposure to ambient tobacco smoke is estimated to produce about 5000 lung cancer deaths per year in U.S. nonsmokers aged ≥ 35 yr, with an average loss of life expectancy of 17 ± 9 yr per fatality. The estimated risk to the most-exposed passive smokers appears to be comparable to that from pipe and cigar smoking. Mortality from passive smoking is estimated to be about two orders of magnitude higher than that estimated for carcinogens currently regulated as hazardous air pollutants under the federal Clean Air Act.     

Indoor air exposure to coal and wood combustion emissions associated with a high lung cancer rate in Xuan Wei, China

Residents of Xuan Wei County in China have unusually high lung cancer mortality that cannot be attributed to tobacco use or occupational exposure. They are exposed to smoke from unvented, open pit coal or wood fires (often used for cooking and heating). The variation in lung cancer rates among communes within the county suggests that indoor combustion of smoky coal may be the prime determinant of lung cancer. To characterize the air in Xuan Wei homes, samples of air particles and semivolatile organic compounds were collected from homes located in two communes; one commune has a high rate of lung cancer, and the other has a low rate. Samples collected in the commune where the lung cancer rate is high and where smoky coal is the predominant fuel contained high concentrations of small particles with high organic content; organic extracts of these samples were mutagenic. Samples from homes in the wood-burning commune, which has a low rate of lung cancer, consisted mostly of larger particles of lower organic content and mutagenicity. The smoky coal sample was a mouse skin carcinogen and was a more potent initiator of skin tumors in comparison to the wood or smokeless coal sample.     

Radionuclides in cigarettes may lead to carcinogenesis via p16 inactivation

It is widely accepted that tobacco smoke is responsible for the vast majority of lung cancers worldwide. There are many known and suspected carcinogens present in cigarette smoke, including α-emitting radioisotopes. Epidemiologic studies have shown that increased lung cancer risk is associated with exposure to ionizing radiation, and it is estimated that the majority of smoking-induced lung cancers may be at least partly attributable to the inhaled and deposited radiation dose from radioisotopes in the cigarette smoke itself. Recent research shows that silencing of the tumor suppressor gene p16^INK4a (p16) by promoter methylation plays a role in smoking-related lung cancer. Inactivation of p16 has also been associated with lung cancer incidence in radiation-exposed workers, suggesting that radionuclides in cigarette smoke may be acting with other compounds to cause smoking-induced lung cancer. We evaluated the mechanism of ionizing radiation as an accepted cause of lung cancer in terms of its dose from tobacco smoke and silencing of p16. Because both radiation and cigarette smoking are associated with inactivation of p16, and p16 inactivation has been shown to play a major role in carcinogenesis, ionizing radiation from cigarette smoke likely plays a role in lung cancer risk. How large a role it plays, relative to chemical carcinogens and other modes of action, remains to be elucidated.     

Pesticide exposure and lung cancer mortality in Leningrad province in Russia

This study was carried out to examine the association between pesticide exposure and lung cancer mortality. We conducted an autopsy based case-control study in Leningrad Province in Russia. A total of 540 lung cancer cases and 582 controls were identified among subjects who had died in the hospitals of the Leningrad province between 1993 and 1998. Using work history records, we assessed exposure to pesticide at the level of industry and job title. Unconditional logistic regression was used to calculate adjusted odds ratio for pesticide exposure and lung cancer mortality. There was no association between ever exposure to pesticide and lung cancer mortality overall (odds ratio=1.06, 95% confidence interval=0.82-1.36) and in both men (odds ratio=1.11, 95% confidence interval=0.84-1.46) and women (odds ratio=0.74, 95% confidence interval=0.37-1.46). We observed no statistically significant odds ratio by duration of pesticide exposure, intensity of pesticide exposure, and cumulative pesticide exposures with lung cancer mortality in both smokers and nonsmokers. Odds ratio also did not differ when the analysis was restricted to individuals who had exposure data with high confidence scores. Our findings suggest no associations between pesticide exposures and mortality of lung cancer in the population of the Leningrad province in Russia that deserves further evaluation.     

Impact of large industrial emission sources on mortality and morbidity in Chile: A small-areas study

Chile suffers significant pollution from large industrial emitters associated with the mining, metal processing, paper production, and energy industries. The aim of this research was to determine whether the presence of large industrial facilities (i.e. coal- and oil-fired power plants, pulp and paper mills, mining facilities, and smelters) affects mortality and morbidity rates in Chile. For this, we conducted an ecological study that used Chilean communes as small-area observation units to assess mortality and morbidity. Public databases provided information on large pollution sources relevant to Chile. The large sources studied were oil- and coal-fired power plants, copper smelters, pulp and paper mills, and large mining facilities. Large sources were filtered by first year of production, type of process, and size. Mortality and morbidity data were acquired from public national databases, with morbidity being estimated from hospitalization records. Cause-specific rates were calculated for the main outcomes: cardiovascular, respiratory, cancer; and other more specific health outcomes. The impact of the large pollution sources was estimated using Bayesian models that included spatial correlation, overdispersion, and other covariates. Large and significant increases in health risks (around 20%–100%) were found for communes with power plants and smelters for total, cardiovascular, respiratory, all-cancer, and lung cancer mortality. Higher hospitalization rates for cardiovascular disease, respiratory disease, cancer, and pneumonia (20–100%) were also found for communes with power plants and smelters. The impacts were larger for men than women in terms of both mortality and hospitalizations. The impacts were also larger when the sources were analyzed as continuous (production volume) rather than dichotomous (presence/absence) variables. In conclusion, significantly higher rates of total cardiovascular, respiratory, all-cancer and lung cancer mortality and cardiovascular, respiratory, cancer and pneumonia hospitalizations were observed in communes with power plants and smelters.     

Enhanced susceptibility to infection in mice after exposure to dilute exhaust from light duty diesel engines

A series of experiments was conducted in which groups of mice were first exposed for various durations to diluted exhaust from light duty diesel engines and then briefly to an infectious aerosol generated by nebulizing cultures of a bacterial pathogen (Streptococcus). Typically, postinfection mortality was significantly greater in groups exposed to exhaust than in their corresponding control groups exposed to purified air only. Data of recent diesel and of past diesel- and catalyst-treated gasoline engine exhaust experiments suggest a somewhat greater excess mortality from (enhanced susceptibility to) bacterial infection in mice exposed to diesel exhaust than in those exposed to catalytic gasoline exhaust. Limited data on acute tests of NO₂ and acrolein vapor alone suggest that the infectivity-enhancing effect of diesel exhaust could be accounted for in large part by these components. Exposures to diesel exhaust, NO₂, or acrolein did not enhance the mortality response to a viral pathogen (A/PR8-34).     

Never smoker lung cancer risks from exposure to particulate tobacco smoke

The average particulate environmental tobacco smoke (ETS) exposure of never and current smokers and the average lung cancer mortality rate for current smokers is estimated from empirical data. These estimates are used in a linear downward extrapolation of the lung cancer risk/mg of particulate ETS exposure for current smokers to calculate the average lung cancer risk for never smokers and the number of never smoker lung cancer deaths (LCD) in the U.S. in 1980 from exposure to particulate ETS. The estimated average daily inhaled particulate ETS exposure for never smokers is 0.62 mg/day for men and 0.28 mg/day for women. The average never smoker is estimated to retain 11% of the inhaled exposure, for a daily retained exposure of 0.07 mg for men and 0.03 mg for women. Other estimates are: a daily retained exposure for current smokers of 310 mg for men and 249 mg for women, a smoking-attributable lung cancer risk for current smokers in 1980 of 284 LCD/100,000 men and 121 LCD/100,000 women, and an annual retained-exposure lung cancer risk for never smokers of 0.64 LCD/100,000 men and 0.015 LCD/100,000 women. These risks and exposures estimate 12 lung cancer deaths among never smokers from exposure to particulate ETS: 8 among the 11.96 million male never smokers and 4 among the 28.85 million female never smokers in the U.S. in 1980. Conversely, between 655 and 3,610 never smoker lung cancer deaths are estimated from methods based on the average lung cancer risk observed in epidemiological studies of exposure to ETS. Three possible reasons for the discrepancy between the exposure and risk-based estimates are discussed: the excess risks observed in epidemiological studies are due to bias, the relationship between exposure and risk is supralinear, or sidestream tobacco smoke is substantially more carcinogenic than an equivalent exposure to mainstream smoke.     

Pulmonary function evaluation of cats after one year of exposure to diesel exhaust

Adult male, inbred, disease-free cats of uniform age and size were exposed eight hours per day, seven days per week to a 1 : 18 dilution of diesel exhaust emissions. After one year of exposure, the animals were removed from the chambers for measurement of lung volumes, forced expiratory flow rates, dynamic compliance and resistance, diffusing capacity, and nitrogen washout. No important changes in pulmonary function were detected with the exception of a decrease in closing volume (P < 0.05). The inability to detect decrements in pulmonary function may have been due to insufficient cocentration of exhaust, insufficient exposure length, or to the use of a species resistant to diesel exhaust. To test these possibilities, the cats are being exposed for an additional year, and another species, hamsters, are being exposed for future testing at exhaust dilutions of 1 : 18 and 1 : 9.     

Pulmonary function testing of animals chronically exposed to diluted diesel exhaust for 267 days

Thw purpose of this work was to assess the potential effect that chronic inhalation of diesel exhaust may have on lung mechanics and lung volumes. Noninvasive pulmonary function tests have been conducted repeatedly on 25 rats exposed to diesel exhaust at a particulate concentration of 1500 μg/m³, for 20 h/day, days/week for 267 days. The same tests were conducted on 25 clean air control animals. When the data is normalized, there are no apparent functionally significant changes occurring in the lungs that may be attributed to the chronic inhalation of diesel exhaust.     

Potential source of asbestos in non-asbestos textile manufacturing company

Recently, a worker with lung carcinoma and a metastatic brain tumor was diagnosed as having a work-related disease. He had been employed in a non-asbestos textile company for 25 years. Consequently, to identify and explore possible causative agents for lung cancer in a non-asbestos textile manufacturing company and establish a causal relationship between exposure and lung cancer, an epidemiological investigative study was conducted and the work processes the worker was engaged in were examined. Air samples were taken from the workplace and during the drilling processes, and a suspected causative material was analyzed. The study revealed that the subject had been employed in the non-asbestos textile manufacturing company for 25 years from 1973 and his responsibilities included repairing spinning machines. In particular, the subject was involved in drilling B-bushings that were used to protect against gear abrasion in the spinning machines. An analysis of the B-bushings using a transmission electron microscope equipped with an energy dispersive X-ray analyzer indicated that they contained crocidolite asbestos fibers. Air samples obtained when drilling the B-bushings clearly indicated that the subject had most likely been exposed to crocidolite fibers when installing the B-bushings in the spinning machines. The frequency and duration of the work suggested that there would be a sufficient degree of exposure to crocidolite fibers to cause lung cancer. Except for smoking and asbestos exposure, no other chemical exposure was suspected for developing lung cancer in the workplace. Smoking appeared to be more of a potentiating risk factor in conjunction with the asbestos exposure. Accordingly, this case may provide significant evidence in identifying the cause of the mesothelioma or lung carcinoma found among workers in non-asbestos textile manufacturing companies elsewhere.     

Health effects and exposure to polychlorinated biphenyls (PCBs) and metals in a contaminated community

Environmental measurements carried out by local authorities during the 1970s, 80s and 90s in an area contaminated by hundreds of years of industrial activities have revealed high levels of zinc (Zn), copper (Cu), lead (Pb) and cadmium (Cd) in soil, vegetables, root crops, berries and mushrooms. In 1972, a large quantity of oil contaminated with polychlorinated biphenyls (PCBs) was accidentally spilled into the river running through the village. To investigate the possible health effects of exposure from local sources, all cancer diagnoses, registered in 1960–2003 for individuals living in the study area, were collected from the regional cancer register of southeast Sweden. The total cancer incidence was non-significantly decreased both among males and females as compared to national rates (SIR = 0.91) for each gender. Among males, increased risks, of border-line significance, were seen for testicular cancer and lymphomas as well as significantly decreased risks for cancer in the rectum, respiratory system and brain. Information on lifetime residence, occupation, smoking habits, diseases, childbirth and food consumption, was collected via questionnaires from cancer cases and randomly selected controls. In both genders combined, significant associations were found for total cancer and high consumption of local perch, and for lymphomas and high consumption of both perch and pikeperch. Female breast cancer was significantly associated with high consumption of local perch and pike as well as with work in metal production. Mothers residing in the parish before the age of five reported significantly more preterm child deliveries. In spite of study limitations, the results indicate that residing in a rural contaminated area may contribute to the development of certain cancers and reproductive effects. In females, high consumption of local fish was shown to be the strongest determinant for total cancer, while in males, the strongest determinant was residing in the study area the first five years of life. Further research including validation of exposure using biomarkers is required to verify the findings as well as future studies in other polluted areas in Sweden with larger population bases.     

Detection and average content levels of carcinogenic and mutagenic compounds from the particulates on diesel and gasoline engine mufflers

Carcinogenic and mutagenic compounds, which were extracted from the particulates that adhered to inner surfaces of diesel and gasoline engine mufflers, were quantified by the series method of Soxhlet extraction, liquid-liquid partition, thin-layer chromatography, and spectrofluorometry. Mutagenic activity of their neutral and acidic fractions was tested in the improved Ames assay by the preincubation method with Salmonella typhimurium TA98 in the presence and absence of metabolic activation system (S-9 mix). The average content levels (μg/g tar) of polycyclic aromatic hydrocarbons from gasoline engine cars were greater than those from diesel engine vehicles. However, the levels of nitro derivatives of PAHs and polycyclic quinones from the diesel engines were greater than from the gasoline engines. Mutagenic activity of the diesel acidic fraction was the highest among the diesel and gasoline fractions, and was significantly higher in the absence of the S-9 mix. Furthermore, the relative value (R_{c = 0}) of infrared absorption of carbonyl stretching vibration to that of methylene asymmetric stretching vibration of the diesel acidic fraction was the highest among the diesel and gasoline fractions. These results strongly suggest that highly direct-acting mutagens in the acidic fraction are at higher levels in diesel emission particulates than those from gasoline, and that these mutagens are carboxylic acid, aldehyde, and alcohol derivatives of PAHs and NPAHs.     

Pulmonary function changes in Chinese hamsters exposed six months to diesel exhaust

Chinese hamsters were exposed for eight hours per day to automotive diesel exhaust emissions which were diluted with air (18 to 1) and had a particulate level of 6.4 mg/m³. Pulmonary function measurements were made after six months exposure. Body weight (BW), lung weight (LW), vital capacity (VC), residual volume by water displacement (RV_w) and by gas dilution (RV_D), alveolar volume (V_A), and carbon monoxide transfer factor (D_LCO) were measured. LW showed a significant increase in the diesel exposed animals (P < 0.01) while VC, RV_W, and D_LCO showed decreases (P < 0.01). Static deflation volume-pressure curves showed depressed deflation volumes for diesel exposed animals when volumes were corrected for body weight and even greater depressed volumes when volumes were corrected for lung weight. However, when volumes were expressed as percent vital capacity, the diesel exposed animals had higher lung volumes at 0 and 5 cm H₂O. Results of the pathological examination of the lung tissue will be necessary for final analysis of our findings. However, preliminary interpretation indicates possible emphysematous changes which are compatible with the observed decrease in D_LCO.     

Deposition and biological availability of diesel particles and their associated mutagenic chemicals

To estimate the human health risk of inhaled diesel particles, it is necessary to know their deposition and retention in the respiratory tract and the rate of dissociation of mutagenic compounds associated with the particles. The deposition of a chain aggregate aerosol of ⁶⁷Ga₂O₃ with size and shape characteristics similar to diesel exhaust particles has been evaluated using Beagle dogs. Approximately one-third of the inhaled activity is deposited in the respiratory tract with most of the particles deposited in the lung. The mutagenic activity present in dichloromethane, dog serum, dog lung lavage fluid, saline, dipalmitoyl lecithin (DPL) and albumin following incubation of these fluids with diesel exhaust particles was determined in the Ames Salmonella system. As observed by other investigators, large quantities of mutagenic activity were removed by dichloromethane. A very small amount of mutagenic activity was removed by the serum and lavage fluid over a 3-day incubation period. No activity was detected following elution with the other solvents. The finding that minimal mutagenic activity could be demonstrated in the biological media following incubation with diesel exhaust particles may be due to a lack of removal of mutagens from the particles or an inactivation of removed mutagens by protein binding or other processes.     

Cancer mortality in towns in the vicinity of incinerators and installations for the recovery or disposal of hazardous waste

BackgroundWaste treatment plants release toxic emissions into the environment which affect neighboring towns.ObjectivesTo investigate whether there might be excess cancer mortality in towns situated in the vicinity of Spanish-based incinerators and installations for the recovery or disposal of hazardous waste, according to the different categories of industrial activity.MethodsAn ecologic study was designed to examine municipal mortality due to 33 types of cancer, across the period 1997–2006. Population exposure to pollution was estimated on the basis of distance from town of residence to pollution source. Using Besag–York–Mollié (BYM) regression models with Integrated Nested Laplace approximations for Bayesian inference, and Mixed Poisson regression models, we assessed the risk of dying from cancer in a 5-kilometer zone around installations, analyzed the effect of category of industrial activity, and conducted individual analyses within a 50-kilometer radius of each installation.ResultsExcess cancer mortality (BYM model: relative risk, 95% credible interval) was detected in the total population residing in the vicinity of these installations as a whole (1.06, 1.04–1.09), and, principally, in the vicinity of incinerators (1.09, 1.01–1.18) and scrap metal/end-of-life vehicle handling facilities, in particular (1.04, 1.00–1.09). Special mention should be made of the results for tumors of the pleura (1.71, 1.34–2.14), stomach (1.18, 1.10–1.27), liver (1.18, 1.06–1.30), kidney (1.14, 1.04–1.23), ovary (1.14, 1.05–1.23), lung (1.10, 1.05–1.15), leukemia (1.10, 1.03–1.17), colon–rectum (1.08, 1.03–1.13) and bladder (1.08, 1.01–1.16) in the vicinity of all such installations.ConclusionsOur results support the hypothesis of a statistically significant increase in the risk of dying from cancer in towns near incinerators and installations for the recovery or disposal of hazardous waste.     

Brain cancer associated with environmental lead exposure: Evidence from implementation of a National Petrol-Lead Phase-Out Program (PLPOP) in Taiwan between 1979 and 2007

Background and objectiveIn 1981, a Petrol-Lead Phase-Out Program (PLPOP) was launched in Taiwan for the abatement of environmental lead emissions. The present study was intended to examine whether the high Petrol-Lead Emission Areas (PLEA) would result in an increase in the incidence rate of brain cancer based on a national data bank.MethodsThe national brain cancer incidence data was obtained from the Taiwan National Cancer Registry. Age standardized incidence rates were calculated based on the 2000 WHO world standard population, and gasoline consumption data was obtained from the Bureau of Energy. The differences in the trend tests for age-standardized incidence rates of brain cancer between high, median, low, and small PLEA were analyzed.ResultsA significant increase was found from small to high PLEA in age-standardized incidence rates of brain cancer. By taking six possible confounders into account, the age-standardized incidence rates for brain cancer were highly correlated with the median and high PLEA by reference to the small PLEA.ConclusionAfter being adjusted for a number of relevant confounders, it could be concluded that high PLEA might result in an increase in the incidence rate of brain cancer resulting from high lead exposures.     

Particle size measurements of automotive diesel emissions

The automative diesel engine has long been acknowledged as being “dirtier” than the spark ignition engine and its particulate emissions may be carcinogenic. Possible solutions to the diesel emission problem are combustion modification or aftertreatment devices. Selection of candidate aftertreatment devices requires knowledge of the physical and chemical properties of the particles, including particle morphology, size distribution, mass concentration and emission rates in the exhaust gas stream. The study reported here represents the first of a series of experiments designed to characterize the exhaust emissions and test various aftertreatment devices. This paper deals only with the particulate characterization phase of the program. Results of size distribution, particle concentration and mass emission rate measurements for a 5.71 displacement Oldsmobile diesel engine are given for a variety of engine operating conditions.     

Polonium-210 budget in cigarettes

Due to the relatively high activity concentrations of (210)Po and (210)Pb that are found in tobacco and its products, cigarette smoking highly increases the internal intake of both radionuclides and their concentrations in the lung tissues. That might contribute significantly to an increase in the internal radiation dose and in the number of instances of lung cancer observed among smokers. Samples of most frequently smoked fine and popular brands of cigarettes were collected from those available on the Egyptian market. (210)Po activity concentrations were measured by alpha spectrometry, using surface barrier detectors, following the radiochemical separation of polonium. Samples of fresh tobacco, wrapping paper, fresh filters, ash and post-smoking filters were spiked with (208)Po for chemical recovery calculation. The samples were dissolved using mineral acids (HNO(3), HCl and HF). Polonium was spontaneously plated-out on stainless steel disks from diluted HCl solution. The (210)Po activity concentration in smoke was estimated on the basis of its activity in fresh tobacco and wrapping paper, fresh filter, ash and post-smoking filters. The percentages of (210)Po activity concentrations that were recovered from the cigarette tobacco to ash, post-smoking filters, and smokes were assessed. The results of this work indicate that the average (range) activity concentration of (210)Po in cigarette tobacco was 16.6 (9.7-22.5) mBq/cigarette. The average percentages of (210)Po content in fresh tobacco plus wrapping paper that were recovered by post-smoking filters, ash and smoke were 4.6, 20.7 and 74.7, respectively. Cigarette smokers, who are smoking one pack (20 cigarettes) per day, are inhaling on average 123 mBq/d of (210)Po and (210)Pb each. The annual effective doses were calculated on the basis of (210)Po and (210)Pb intake with the cigarette smoke. The mean values of the annual effective dose for smokers (one pack per day) were estimated to be 193 and 251 microSv from (210)Po and (210)Pb, respectively.     

Selenium and exposure to fibrogenic mineral dust: A mini-review

Individuals exposed to fibrogenic mineral dust may exhibit an impaired antioxidant system and produce high levels of reactive oxygen and nitrogen species through immune cells, contributing to the perturbation of immune cell function, inflammation, fibrosis and lung cancer. The lung diseases which are caused by inhalation of fibrogenic mineral dust, known as pneumoconioses, develop progressively and irreversibly over decades. At the moment there is no known cure. The trace element selenium has potent antioxidant and anti-inflammatory properties mediated mainly through selenoproteins. Research has demonstrated that selenium has the ability to protect against cardiovascular diseases; to kill cancer cells in vitro and reduce cancer incidence; and to immunomodulate various cellular signaling pathways. For these reasons, selenium has been proposed as a promising therapeutic agent in oxidative stress associated pathology that in theory would be beneficial for the prevention or treatment of pneumoconioses such as silicosis, asbestosis, and coal worker's pneumoconiosis. However, studies regarding selenium and occupational lung diseases are rare. The purpose of this study is to conduct a mini-review regarding the relationship between selenium and exposure to fibrogenic mineral dust with emphasis on epidemiological studies. We carried out a systematic literature search of English published studies on selenium and exposure to fibrogenic mineral dust. We found four epidemiological studies. Reviewed studies show that selenium is lower in individuals exposed to fibrogenic mineral dust. However, three out of the four reviewed studies could not confirm cause-and-effect relationships between low selenium status and exposure to fibrogenic mineral dust. This mini-review underscores the need for large follow-up and mechanistic studies for selenium to further elucidate its therapeutic effects.