Pulmonary metal distribution in urban dwellers

Tsuchiyama, Fumi; Hisanaga, Naomi; Shibata, Eiji; Aoki, Takeshi; Takagi, Hiromi; Ando, Tatsushi; Takeuchi, Yasuhiro

doi:10.1007/s004200050190

Cited by 30 publications

(20 citation statements)

References 17 publications

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“…Elevated blood lead levels in U.S. children have also been associated with second-hand smoke exposure. 82 Lead concentrations have also been reported to be significantly higher in four of five lobes of smokers' lungs, 46 indicating accumulation in smokers' lungs also. Lead has been reported at higher concentrations in the exhaled breath condensate of study subjects with COPD, than that of the nonsmoking control subjects and in current normal smokers vs. nonsmokers.…”

Section: Leadmentioning

confidence: 99%

“…45 Chromium concentrations have been reported to be significantly higher in all five lobes of smokers' lungs than in nonsmokers' lungs. 46 However, it is not clear in what proportions chromium (III) and chromium (VI) accumulate. Data to date have been based on analyses of chromium (III) and chromium (VI) by difference in two methods, in cigarette ash, or before and after reduction.…”

Section: Chromiummentioning

confidence: 99%

“…Nickel concentrations have been reported to be significantly higher in all five lobes of smokers' lungs compared to nonsmokers' lungs. 46 Nickel has been reported as present in significantly higher concentrations in placenta samples of smokers than in placenta of non-smokers, 53 affirming systemic absorption from the lungs.…”

Section: Nickel and Cobaltmentioning

confidence: 99%

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Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

2011

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Biochemically and pathologically, there is strong evidence for both atopic and nonatopic airway sensitization, hyperresponsiveness, and inflammation as a consequence of exposure to tobacco mainstream or sidestream smoke particulate. There is growing evidence for the relation between exposure to mainstream and sidestream smoke and diseases resulting from reactive oxidant challenge and inflammation directly as a consequence of the combined activity of neutrophils, macrophages, dendritic cells, eosinophils, basophils, as a humoral immunological consequence of sensitization, and that the metal components of the particulate play a role in adjuvant effects. As an end consequence, carcinogenicity is a known outcome of chronic inflammation.Smokeless tobacco has been evaluated by the IARC as a group 1 carcinogen. Of the many harmful constituents in smokeless tobacco, oral tissue metallothionein gradients suggest that metals contribute to the toxicity from smokeless tobacco use and possibly sensitization.This work reviews and examines work on probable contributions of toxic metals from tobacco and smoke to pathology observed as a consequence of smoking and the use of smokeless tobacco. Metals and metalloids in tobaccoThough exposure to substances from tobacco use is obviously a complex exposure, the carcinogens in tobacco smoke have been classified for health risk determinations into five major chemical classes. 1 Some of these have been carefully studied, contributing to a strong weight of evidence for associated health risks. 2 Toxic metals and metalloids constitute one of the more understudied major carcinogenic chemical classes in smokeless tobacco products and tobacco smoke. Eight of the top forty substances in the Fowles and Dybing table of cancer risk indices are metals or metalloid compounds. 1 In their table of non-cancer risk indices for individual chemical constituents of mainstream cigarette smoke based on a single cigarette per day, three of the top eight listed for respiratory effect health risk, cadmium, hexavalent chromium, and nickel, were metals. Another metalloid, silicon in the form of silicates, poses serious health risks by inhalation, but limited data is available, likely due to analytical difficulties.Metals and metalloids in smoke from biomass combustion including tobacco are generally considered to be present in ionic form, but may also occur in a gaseous elemental form, as is the case for mercury. 3 Whether a tobacco product is consumed by smoking or in a smokeless form, the exposure to toxic metals is directly related to the concentration in the tobacco leaf, assuming no metal containing additives are included during manufacture. [4][5][6] The soil (including any amendments to the soil such as sludge, fertilizers, or irrigation with

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Section: Leadmentioning

confidence: 99%

Section: Chromiummentioning

confidence: 99%

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Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

2011

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“…Another study of urban dwellers (n = 17) demonstrated an average of 0.22-1.93 pg nickel/g dry weight of lung tissue, with the highest concentration in the upper lobes. Cigarette smoking and a history of occupational exposure significantly increased levels (180).…”

Section: Metal Fume Fevermentioning

confidence: 99%

Inorganic dust pneumonias: the metal-related parenchymal disorders.

Kelleher

Pacheco

Newman

2000

Environ Health Perspect

150

117

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In recent years the greatest progress in our understanding of pneumoconioses, other than those produced by asbestos, silica, and coal, has been in the arena of metal-induced parenchymal lung disorders. Inhalation of metal dusts and fumes can induce a wide range of lung pathology, including airways disorders, cancer, and parenchymal diseases. The emphasis of this update is on parenchymal diseases caused by metal inhalation, including granulomatous disease, giant cell interstitial pneumonitis, chemical pneumonitis, and interstitial fibrosis, among others. The clinical characteristics, epidemiology, and pathogenesis of disorders arising from exposure to aluminum, beryllium, cadmium, cobalt, copper, iron, mercury, and nickel are presented in detail. Metal fume fever, an inhalation fever syndrome attributed to exposure to a number of metals, is also discussed. Advances in our knowledge of antigen-specific immunologic reactions in the lung are particularly evident in disorders secondary to beryllium and nickel exposure, where immunologic mechanisms have been well characterized. For example, current evidence suggests that beryllium acts as an antigen, or hapten, and is presented by antigen-presenting cells to CD4+ T cells, which possess specific surface antigen receptors. Other metals such as cadmium and mercury induce nonspecific damage, probably by initiating production of reactive oxygen species. Additionally, genetic susceptibility markers associated with increased risk have been identified in some metal-related diseases such as chronic beryllium disease and hard metal disease. Future research needs include development of biologic markers of metal-induced immunologic disease, detailed characterization of human exposure, examination of gene alleles that might confer risk, and association of exposure data with that of genetic susceptibility. Key words: aluminum, beryllium, cadmium, cobalt, copper, hard metal disease, iron, mercury, metal fume fever, nickel, pneumoconiosis. The term pneumoconiosis, first introduced in the 19th century, refers to diseases and pathologic consequences from inhalation of particulate dusts. In recent years the greatest progress in our understanding of pneumoconioses, other than those produced by asbestos, silica, and coal, has been in the arena of metalinduced parenchymal lung disorders. As presented in Table 1 (1). A major theme that emerges in reviewing recent developments in metal-related lung toxicity is the extent to which various metals are capable of inducing both antigen-specific immunologic reactions in the lung and nonspecific "innate" immune system responses characterized by inflammation frequently triggered by oxidant injury. With the recognition of these immune and inflammatory effects comes a growing awareness of the potential hazards to the lung at low levels of exposure. There is also increasing research being conducted on the interaction between metal exposure and the human genome. In the cases of beryllium and cobalt, for example, there is emerging recognition of the spec...

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“…Such differentiation is lost when bulk samples of tissue are used to quantify the retained lung burden (Tsuchiyama et al 1997). Two basic particle forms were identified in the electron microscope.…”

mentioning

confidence: 99%

Toxicologic and epidemiologic clues from the characterization of the 1952 London smog fine particulate matter in archival autopsy lung tissues.

Hunt

Abraham

Judson

et al. 2003

Environ Health Perspect

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Exposure to atmospheric fine particulate matter (PM), even at low ambient concentrations, has clearly been linked to increases in mortality and morbidity. A 10- micro g m(-3) increase in PM10 (PM < 10 micro m) has been found to produce a 0.5% increase in daily mortality. The mechanism of action is a source of debate, although recent attention has focused on the cardiac effects of PM exposures. Likewise, several possible etiologic agents have been implicated, including ultrafine PM (PM

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Pulmonary metal distribution in urban dwellers

Cited by 30 publications

References 17 publications

Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

Inorganic dust pneumonias: the metal-related parenchymal disorders.

Toxicologic and epidemiologic clues from the characterization of the 1952 London smog fine particulate matter in archival autopsy lung tissues.

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