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Risk of lung cancer from environmental exposures to tobacco smoke.

Epidemiologic evidence on the relation between environmental tobacco smoke and cancer is reviewed. The labeling of tobacco smoke as an environmental cause of lung cancer has been challenged based on allegations of bias in the epidemiologic data. However, tobacco smoke has been shown to increase the risk of lung cancer down to the lowest exposure levels. Environmental tobacco smoke contains the same carcinogenic compounds as those found in the tobacco smoke inhaled directly by the smoker. Nonsmokers environmentally exposed have elevated levels of tobacco smoke byproducts in biological samples. These observations alone are sufficient to identify tobacco smoke as an environmental carcinogen. The epidemiologic studies showing that environmental exposure to tobacco smoke is associated weakly but consistently with increased risk of lung cancer. While these epidemiologic studies have been challenged, it does not appear that the observed epidemiologic associations are due to misclassification or confounding. Indeed, the epidemiologic results, particularly among the studies with superior data collection methods and better control of bias and confounding, find consistent associations between environmental tobacco smoke and lung cancer. This paper summarizes the evidence that environmental exposure to tobacco smoke increases the risk of lung cancer, and considers the criticisms of the epidemiologic evidence which have been raised.

Bias↗

[A study on risk of malignant neoplasm and environmental exposure to crocidolite].

OBJECTIVE: To explore the risk of developing malignant neoplasm in a cohort with the history of environmental exposure to crocidolite asbestos. METHODS: A retrospective cohort and follow-up study covering 15 years (1987 --> 1995 --> 2001) was carrid out in a small town in Yunnan province. The cohort comprised 6254 local inhabitants. The deaths from and the RR of asbestos-related malignant neoplasms were studied. RESULTS: There were 186 deaths from neoplasms in the observation group, the mortality being 2160.5 per 10(6) person-years (RR=1.293, 95%CI: 1.032-1.618), 20 of those deaths were caused by mesothelioma, with a crude mortality of 232.3 per 10(6) person-years (RR=17.929; 95%CI: 2.406-133.592). The mortalities for men and women were 267.5 and 186.7 per 10(6) person-years respectively. The crude mortality from lung cancer (56 deaths) was 650.5 per 10(6) person-years,there is no significance between the two groups (RR=1.434; 95%CI: 0.968-2.486). The difference in mortality from gastrointestinal cancer between the two groups is not significant, whereas the risk of man intestinal cancer in the observation is significant (RR=3.71; 95%CI: 1.077-13.270). CONCLUSION: The risk of developing mesothelioma is significantly increased in the population with environmental exposure to crocidolite. The risk of man intestinal cancer in the town awaits additional studies.

Adult↗

Environmental exposure and preventive measures in Sweden and EU.

Environmental exposure to cadmium (Cd) gives rise to renal tubular dysfunction at low cumulative doses of Cd. A possible role of Cd in influencing the occurrence of diseases, e.g., bone, reproductive and cancer in the general population groups environmentally exposed to Cd has been reported from Japan, Belgium, Sweden and China. Authorities have to pay attention to this fact and to act in order to prevent serious outcomes and personal suffering in the population groups at risk. A general approach in setting recommended health based limits and to regulate the occurrence of a substance existing in food stuff is to keep low levels -better to be on the safer side than on the risk side. In the case of cadmium it should be most clear that since cadmium has a very long biological half-life of 20 years in humans, increased cadmium exposure due to human activities can never be accepted. In cases where cadmium exposure can not be avoided the approach should be to limit and decrease exposure. Presently FAO/WHO Expert Committee on Food Additives and Food has a PTWI (provisional tolerable weekly intake) value for adult persons of 7 microg/kg body weight for Cd (WHO 2003) a value corresponding to 1 microg/kg body weight for each day of a week. For children and pregnant or lactating women daily intakes should not exceed 1 microg/kg body weight.

Cadmium↗

Health effects of environmental exposure to cadmium in a population study.

The Cadmibel Study is a cross-sectional population study, which investigated the hypothesis that environmental exposure of the population to cadmium would result in health effects. The 2,327 participants constituted a random sample of the population of four Belgian districts, chosen to provide a wide range of environmental exposure to cadmium. The urinary cadmium excretion, a measure of lifetime exposure, averaged 9.3 nmol/24h in men (range 0.4-325 nmol/24h) and 7.2 nmol (0.1-71 nmol/24h) in women. The Cadmibel Study refuted the hypothesis that exposure to cadmium would lead to an increase in BP and in the prevalence of hypertension and other cardiovascular diseases. Serum alkaline phosphatase activity and the urinary excretion of calcium correlated significantly and positively with urinary cadmium in both sexes. These findings suggest that the calcium metabolism is gradually affected, as cadmium accumulates in the body. Furthermore, several markers of renal tubular function (urinary excretion of retinol binding protein, N-acetyl-beta-glucosaminidase, beta 2-microglobulin and aminoacids) were significantly and positively associated with urinary cadmium. There was a 10% probability of abnormal values of these markers of tubular function when urinary cadmium exceeded +/- 20 nmol/24h. However, the morbidity associated with the functional changes, observed in the Cadmibel Study, remains presently unknown and requires further investigation, preferably in a longitudinal population studies.

Adult↗

Environmental exposure unit: a system to test anti-allergic treatment.

LEARNING OBJECTIVES: Reading this article will enable readers to recognize the Environmental Exposure Unit (EEU), its historic development and its current role as a system to test anti-allergic treatment; to recognize clinical relevance of this test system and its relationship with other pollen challenge methods of evaluation of anti-allergic medication; and, to recognize variables associated with standard clinical studies of anti-allergic medication. Readers will review four studies of antihistamines tested in the Environmental Exposure Unit, three studies on nasal corticosteroids, one on topical eye drops and one on immunotherapy conducted in the EEU. DATA SOURCES: The EEU has been in operation since 1985 preceded by a prototype challenge system to assess respiratory effects of urea formaldehyde foam insulation. A number of studies on the onset of action and efficacy of different antihistamines and nasal corticosteroids as well as other treatments have been completed producing accurate and consistent results influenced to some extent by study designs. STUDY SELECTION: Studies of commonly used antihistamines and nasal corticosteroids are discussed in detail and represent several of the studies undertaken to date in the EEU. RESULTS: Controlled ragweed pollen exposure using the EEU has shown that some antihistamines demonstrate an onset of action within 30 minutes while others have taken up to 3 hours to produce significant effect. Nasal corticosteroids evidenced the onset of clinical improvement at 5 to 6 hours with significance over placebo between 6 and 12 hours depending on dose. CONCLUSION: The EEU is an effective pollen delivery system that accurately and consistently determines the onset of action and efficacy of anti-allergic treatment in large groups of subjects. It eliminates variables associated with various other methods of evaluation of these medications but does not supplant the need for such evaluations.

Anti-Allergic Agents↗

Evaluation of uncontrolled confounding in studies of environmental exposures and neurobehavioral testing in children.

BACKGROUND: Neurobehavioral tests are commonly used in studies of children exposed to low-level environmental concentrations of compounds known to be neurotoxic at higher levels. However, uncontrolled or incomplete control for confounding makes interpretation of results problematic because effects of confounders are often stronger than the effects of primary interest. We examined a priori the potential impact of confounding in a hypothetical study evaluating the association of a potentially neurotoxic environmental exposure with neurobehavioral function in children. METHODS: We used 2 outcome measures: the Bayley Scales of Infant Development Mental Development Index and the Stanford-Binet Intelligence Scale Composite Score. We selected 3 potential confounders: maternal intelligence, home environment, and socioeconomic status as measured by years of parental education. We conducted 3 sets of analyses measuring the effect of each of the 3 confounding factors alone, 2 confounders acting simultaneously, and all 3 confounders acting simultaneously. RESULTS: Relatively small differences (0.5 standard deviations) in confounding variables between "exposed" and "unexposed" groups, if unmeasured and unaccounted for in the analysis, could produce spurious differences in cognitive test scores. The magnitude of this difference (3-10 points) has been suggested to have a meaningful impact in populations. The method of measuring confounders (eg, maternal intelligence) could also substantially affect the results. CONCLUSIONS: It is important to carefully consider the impact of potential confounders during the planning stages of an observational study. Study-to-study differences in neurobehavioral outcomes with similar environmental exposures could be partially explained by differences in the adjustment for confounding variables.

Bias↗

Male infertility and environmental exposure to lead and cadmium.

Humans are exposed occupationally and environmentally to metal aerosols including lead (Pb2+) and cadmium (Cd2+). These toxicants accumulate in male reproductive organs. Epidemiological studies have been equivocal about effects of Pb2+ and Cd2+ on hormone concentrations, male fertility and sperm parameters. Comparison of Pb2+ and Cd2+ concentrations in fertile and infertile men are problematic. Problem areas include failure to control confounding variables, but genetic polymorphisms as in somatic diseases may modulate Pb2+ and Cd2+ damage. Multiple calcium (Ca2+) and potassium (K+) channel isoforms have been identified in human testes and spermatozoa. These Ca2+ and K+ channels are involved in early events of acrosome reactions. Ca2+ channel are susceptible to Cd2+ poisoning and K+ channels to Pb2+. These channels offer entry paths for metallic toxicants into mature spermatozoa. Ion channel polymorphisms may cause differential sensitivities to Cd2+ and Pb2+, explaining in part prospective blinded studies showing high Cd2+ in varicocele-related human infertility and high Pb2+ in unexplained infertility. In both forms of male infertility the ability to undergo an acrosome reaction decreases. Reverse transcriptase-polymerase chain reaction assays for Ca2+ and K+ channel isoforms may identify susceptibility subgroups with lower resistance to environmental exposures.

Cadmium↗

Mortality from cancer of the male reproductive tract and environmental exposure to the anti-androgen p,p'-dichlorodiphenyldichloroethylene in the United States.

The association of prostate cancer mortality and testicular cancer mortality with environmental exposure to the anti-androgen dichlorodiphenyltrichloroethane (DDT) derivative p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) in the USA was explored in the period 1971-1994 using multiple linear regression analysis. Environmental p,p'-DDE contamination by state was estimated by p,p'-DDE concentrations in the subcutaneous fat of population samples and by measurements of p,p'-DDE in tree bark. On average, African Americans had adipose p,p'-DDE levels 74% higher than Whites (8.49 vs. 4.88 microg/g; p < 0.001). Neither prostate cancer mortality nor testicular cancer mortality showed a positive association with either indicator of p,p'-DDE environmental contamination. On the contrary, the regression coefficient for prostate cancer was constantly inverse for adipose p,p'-DDE along the period of study, although it approached statistical significance only for African Americans in 1981-1985 (P=-0.755; 0.10 > p > 0.05). This ecologic study does not provide support to the hypothesis of a link between environmental exposure to DDT derivatives and cancer of the male reproductive tract.

Adipose Tissue↗

Mesothelioma associated with environmental exposures.

BACKGROUND: The main sources of environmental, non-occupational exposure to asbestos or asbestiform fibres are: a) industrial plants in which asbestos was used in the production process; b) asbestos "in place" (mainly in buildings); c) contaminated soils. The association of these exposures with increasing risk of mesothelioma has been documented since 1960 in many places. OBJECTIVES AND METHODS: The present paper is aimed at describing the main results of studies performed in the locations with soils naturally contaminated with asbestos or asbestiform fibres. Environmental exposure data and asbestos-related health outcomes, mainly mesothelioma, are analyzed through a review of the literature. RESULTS: The sites with asbestos or other mesotheliomatogenous fibres in soils are characterized by low concentration levels of airborne fibres. Furthermore, exposure levels may increase when specific activities are carried out (mainly related to building construction), involving mechanical disturbance of fibre-containing materials. The type of fibres found are mainly amphiboles (tremolite). The population at risk of exposure is the general population, which can be exposed from birth. In these sites, the sex ratio of mesothelioma cases is close to 1.0 and the average age of cases ranges from 50 to 60 years. CONCLUSIONS: Both "natural"and industrial environmental asbestos or asbestiform fibre exposures increase potential risk for mesothelioma. Strategies of environmental reclamation and risk communication should be implemented in these areas.

Asbestos↗

Osmium: an appraisal of environmental exposure.

In the U.S., the chief source of new osmium is copper refining, where this metal is produced as a byproduct. Probably less than 10% of the osmium in the original copper ore is recovered, and 1000-3000 oz troy of osmium is lost each year to the environment as the toxic, volatile tetroxide from copper smelters. In 1971, about 2000 oz troy of osmium was domestically refined, most of which was from secondary sources. An additional 4169 oz troy of osmium was toll-refined. Major uses for osmium tetroxide identified are for catalysis, especially in steroid synthesis, and for tissue staining. Minor uses of osmium metal are for electrical contacts and for imparting hardness to alloys for mechanical pivots, etc. Unreclaimed osmium tetroxide that reaches wastewater streams is probably rapidly reduced by organic matter to nontoxic osmium dioxide or osmium metal, which would settle out in the sediment of the water course. Waste osmium metal, itself innocuous and chemically resistant, would be oxidized to the toxic tetroxide if incinerated. Because of the small amounts used and their wide dispersal, the amounts of osmium tetroxide in wastewater and air should pose no hazard to man or the environment. The chief acute toxic effects of osmium tetroxide are well known and include eye and respiratory-tract damage. Few data are available that provide information on possible effects of nonacute exposure resulting from environmental contamination by osmium. However, workers continually exposed to osmium tetroxide vapors (refiners and histologists) and rheumatoid arthritis patients who have received intra-articular injections of osmic acid solutions have shown no apparent damage from exposure to low levels of osmium.

Animals↗

[Evaluation of the effect of environmental exposure to tobacco smoke on variability of peak expiratory flow rate in children].

A panel study was conducted in autumn (116 children) and repeated in spring (66 children) to test the hypothesis that the individual variability of peak expiratory flow rate (PEFR) depends on the environmental exposure to tobacco smoke (ETS). PEFR was measured twice a day (morning: PEFR-M; evening: PEFR-E), using individual meters at homes, in children exposed (ETS+) and not exposed (ETS-) to tobacco smoke at home. In examined groups the individual variability of PEFR-M was--on average--8.0% (ETS+; autumn), 8.1% (ETS+; spring), 10.5% (ETS-; autumn) and 7.7% (ETS-; spring). The individual variability of PEFR-E was 8.0% (ETS+; autumn), 7.9% (ETS+; spring), 9.5% (ETS-; autumn) and 7.4% (ETS-; spring). The results of multivariate analysis of within- and between-subject variability showed the presence of statistically significant within-subject variability only in ETS+ group (PEFR-M in autumn; PEFR-M and PEFR-E in spring). With all the limitations of a panel study design the findings suggest that environmental exposure to tobacco smoke in children affects the degree of within-subject variability of PEFR in children.

Child↗

Contact dermatitis and urticaria from environmental exposures. Agency for Toxic Substances and Disease Registry.

Dermatitis accounts for about 30 percent of all illnesses in the workplace. A thorough exposure history is the most important element in accurate diagnosis of skin lesions. In certain cases, skin lesions may be valuable diagnostic clues to the presence of systemic toxicity. Irritant and allergic contact dermatitis, photosensitivity contact dermatitis, and contact urticaria are examples of skin lesions that may be caused by exposure to an environmental agent.

Adult↗

Occupational styrene exposure: environmental and biological monitoring.

Occupational exposure to styrene was studied by environmental and biological monitoring in 22 workers employed in a fiberglass reinforced plastic factory. The mean environmental styrene concentration in individual workplaces ranged from 120 to 684 microliter/l. Blood styrene, which was tested at the end of the work shift, ranged from 450 to 3700 micrograms/l. Urinary mandelic and phenylglyoxylic acid, which were determined at the end of the work shift, ranged from 133 to 2100 and from 107 to 685 mg/l, respectively. Environmental styrene exposure was better correlated with styrenemia than with mandelicuria and phenylglyoxylicuria considered either individually or together. The ratio between environmental and blood styrene showed that styrenemia was, on average, 3.3-4.9 times higher than environmental styrene concentration.

Air↗

Does environmental exposure to manganese pose a health risk to healthy adults?

Manganese is an essential nutrient that also may be toxic at high concentrations. Subjects chronically exposed to manganese-laden dust in industrial settings develop neuropsychological changes that resemble Parkinson's disease. Manganese has been proposed as an additive to gasoline (as a replacement for the catalytic properties of lead), which has generated increased research interest in the possible deleterious effects of environmental exposure to manganese. Low-level exposure to manganese has been implicated in neurologic changes, decreased learning ability in school-aged children, and increased propensity for violence in adults. However, a thorough review of the literature shows very weak cause-and-effect relationships that do not justify concern about environmental exposure to manganese for most of the North American population.

Behavior↗

Environmental exposure to trace elements and risk of amyotrophic lateral sclerosis: a population-based case-control study.

We analyzed the association between the environmental exposure to trace elements and the risk of sporadic amyotrophic lateral sclerosis (ALS) in a population-based case-control study in the Emilia-Romagna region in northern Italy. We evaluated exposure to selected trace elements by measuring toenail concentrations of the same by means of inductively coupled plasma optical spectrometry and instrumental neutron activation analysis. The final number enrolled in the study was 22 patients and 40 controls. Disease progression, assessed through a clinical score, was generally unassociated with toenail trace element levels, with the exception of an inverse relation with zinc and selenium content and a direct correlation with copper concentration. In logistic regression analysis, we found no evidence of an association between ALS risk and toenail content of cadmium, lead, copper, zinc, manganese, selenium, chromium, cobalt, iron, and aluminum. This investigation does not suggest a major role in sporadic ALS etiology of environmental exposure to these trace elements, though results for zinc, selenium, and copper should be evaluated with caution due to the potential limitations of toenails as biomarkers of chronic exposure in patients.

Amyotrophic Lateral Sclerosis↗

Environmental exposures in elderly Canadians with Parkinson's disease.

BACKGROUND: Etiologic hypotheses for Parkinson's disease have implicated environmental factors, genetic factors, or a combination of the two. METHODS: Data from a survey of elderly Canadians (n = 10,263) with regard to their history of Parkinson's disease and previous environmental exposures were analyzed. Exposure to various environmental factors was compared between 87 patients with Parkinson's disease and 2070 elderly controls without Parkinson's disease. RESULTS: Exposure to plastic resins (OR (odd ratio) = 8.79), epoxy resins (OR = 6.94), glues (OR = 4.26), paints (OR = 3.84), and petroleum (OR = 2.30) products was significantly (p < 0.05) associated with Parkinson's disease. CONCLUSION: These substances deserve further exploration with respect to the possible development of parkinsonism.

Adhesives↗

[The effect of smoking on environmental exposure to carbon of inhabitants in highly and little industrially developed areas].

The aim of the work was an estimation of the effect of smoking on environmental exposure to CO people living in industrial area of Sosnowiec (a city situated in Upper Silesia) and Tomaszów Lubelski (not much industrially town situated at the border of Roztocze National Park). The investigated material was vein blood of 102 blood donors from Sosnowiec and 103 blood donors from Tomaszów Lubelski both smokers and non-smokers. The level of CO exposure was estimated by determination of carbon monoxide haemoglobin (HbCO) concentration in blood by Wolf's method in Antczak's adaptation. It was stated that average HbCO concentration at non-smokers from Sosnowiec (2.09%) was about 0.9% higher than the one at non-smokers from Tomaszów Lubelski (1.17%). An increase of HbCO concentration in blood of non-smokers from Sosnowiec as compared with non-smokers from Tomaszów Lubelski included also 50 and 90 percentile. In relation to 50 percentile it was 2.05 and 1.0% and in relation to 90 percentile 2.4 and 3.7% respectively. The influence of external environment on CO exposure at smokers was estimated on the base of HbCO determination in blood before starting smoking. It was 2.77 at smokers from Sosnowiec and 1.41% at smokers from Tomaszów Lubelski. Analysing the effect of smoking on smokers exposure to CO it was stated that HbCO concentration in blood in both groups increased linearly with the increase of the number of smoked cigarettes, and average increase per one cigarette was 0.43% for smokers from Sosnowiec and 0.57% for smokers from Tomaszów Lubelski. On the base of the obtained results the following conclusions were drawn: 1. industrial and communal environment contamination with carbon monoxide influences considerably the exposure of both smokers and non-smokers. 2. smoking effects significantly more the exposure of people (smokers) to carbon monoxide than environmental pollution in the investigated industrial area. 3. the exposure to carbon monoxide at smokers up with the environmental exposure.

Carbon Dioxide↗