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Carcinogenic and Genetic Effects
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
Carl-Gustaf Elinder, Tord Kjellström
There was a total of 43 deaths between 1949 and 1975.43 Eight of the deaths were caused by cancer, a figure which was not in excess of the expected number based on the total Swedish male population. Cancer morbidity in the battery factory was also investigated. Between 1959 and 1975, 15 cancers had been diagnosed compared to an expected incidence of 16.4, based on data from the Swedish Cancer Register. With regard to specific causes, a significant increase could be shown for cancer of the nasopharynx only — two cases were found — whereas only 0.2 were expected. This was primarily thought to be the result of nickel hydroxide exposure. There was also a tendency for an increased incidence of prostatic, lung, and colorectal cancer, observed cases being 2, 2, and 5, respectively, compared to expected figures of 1.2, 1.4, and 2.2.
Cadmium: Uses, Occurrence, and Intake
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
Cadmium pigments, mainly cadmium sulfide and cadmium sulfoselenide, with colors from yellow to deep red, are used in various types of products, especially plastics, ceramics, and paints. About 60 to 80% of all cadmium pigments produced today is used in the coloring of plastics. The advantages of cadmium pigments are high temperature tolerance and stability to light.42 Certain other compounds, mainly cadmium stearate, are used as stabilizers in plastics, especially in PVC. Cadmium stabilizers inhibit the deterioration processes which take place within the plastic, and which may lead to darkening, hardening, and embrittlement. In rechargeable nickel-cadmium batteries, cadmium hydroxide constitutes one of the electrodes, and nickel hydroxide the other. In larger cells, an alkaline electrolyte is usually employed. Formerly, production was concentrated on the larger cells used in, e.g., aircrafts and locomotives and for lighting and telephone systems. Recently, small cadmium batteries have been developed for use in different types of portable electronic equipment, such as calculators, flashlights, etc. At present, there is a rapidly growing market for small rechargeable cadmium batteries.
Aggravation of atherosclerosis by pulmonary exposure to indium oxide nanoparticles
Published in Nanotoxicology, 2020
Dong-Keun Lee, Hyung Seok Jang, Hyunji Chung, Soyeon Jeon, Jiyoung Jeong, Jae-Hoon Choi, Wan-Seob Cho
Pulmonary exposure to nanoparticles (NPs) can cause a wide range of both acute and chronic lung injuries (Cho et al. 2010). In addition, the presence of NPs in the lung can induce toxicity in secondary organs, including the cardiovascular system (Miller et al. 2017; Mills et al. 2009). Atherosclerosis is a representative cardiovascular disease characterized by hyperlipidemia, chronic vascular inflammation, and lipid accumulation. Previous studies have suggested that the pharyngeal aspiration of diesel exhaust particles (DEP) can aggravate atherosclerosis via a systemic pro-oxidative effect (Bai et al. 2011; Folkmann et al. 2007). Titanium dioxide (TiO2) NPs exerted a modest effect on plaque progression and endothelial dysfunction in ApoE−/− mice (Chen et al. 2013; Mikkelsen et al. 2011). Single-walled carbon nanotubes (SWCNTs) have been shown to induce aortic mitochondrial damage in healthy C57BL/6 mice and accelerate plaque formation in ApoE−/− mice (Li et al. 2007; Suzuki et al. 2016). Multi-walled carbon nanotubes (MWCNTs) showed an accelerated progression of atherosclerosis in ApoE−/− mice (Cao et al. 2014; Christophersen, Jacobsen, Jensen, et al. 2016). A 5-month repeated inhalation exposure to nickel hydroxide NPs in ApoE−/− mice resulted in the exacerbation of atherosclerosis (Kang et al. 2011). However, although the severe pulmonary inflammation caused by nanomaterials has been suggested as a contributory factor in the progression of atherosclerosis, some discrepancies are been found; for example, MWCNTs, a highly inflammogenic nanomaterials, was not found to be correlated with the progression of atherosclerosis (Han et al. 2015).
Electronic cigarette aerosol increases the risk of organ dysfunction by enhancing oxidative stress and inflammation
Published in Drug and Chemical Toxicology, 2022
Kedar N. Prasad, Stephen C. Bondy
Inhalation of nanoparticles of nickel hydroxide induced oxidative stress and inflammation in the lung and heart of mice (Kang et al.2011). In another mouse model, extended exposure to e-cigarette aerosol increased infiltration of inflammatory cells including eosinophils into the airways, stimulated the production of inflammatory cytokines interleukin-4 (IL-4), IL-5 and IL-13 in the lung, and increased airway hyper-responsiveness. In humans, e-cigarettes could in this manner exacerbate allergy-induced asthma (Lim and Kim 2014).
Sex differences in the acute and subchronic lung inflammatory responses of mice to nickel nanoparticles
Published in Nanotoxicology, 2020
Dorothy J. You, Ho Young Lee, Alexia J. Taylor-Just, Keith E. Linder, James C. Bonner
Based on evidence from published epidemiology studies showing that women are generally more susceptible to chronic lung inflammation (Jensen-Fangel et al. 2004; Postma 2007; Gleeson et al. 2011; Kadioglu et al. 2011; Casimir et al. 2013; Pinkerton et al. 2015; Klein and Flanagan 2016), we initially postulated that female mice would be more susceptible to repeated subchronic exposures to NiNPs with or without LPS. However, we observed that male mice were more susceptible to subchronic lung inflammation after repeated exposures to NiNPs and LPS with greater numbers of infiltrating monocytes, whereas NiNPs or LPS alone did not produce a significant increase in monocytes isolated from BALF. This finding is, in part, consistent with a study by Yoshizaki and colleagues (2017) wherein greater numbers of infiltrating monocytes and macrophages were found in the lungs of male mice after repeated subchronic exposure to PM2.5. Furthermore, a retrospective cohort study demonstrated that an increase in monocyte counts in serum was found in patients that developed idiopathic pulmonary fibrosis and other fibrotic disorders (Scott et al. 2019). Several studies have shown that infiltrating monocytes require chemokine receptor CCR2 in order to migrate to inflammatory sites containing high levels of the chemokine ligand CCL2 and that the CCL2/CCR2 signaling pathway is involved in the pathogenesis of bleomycin-induced pulmonary fibrosis (Kurihara and Bravo 1996; Okuma et al. 2004; O’Connor, Borsig, and Heikenwalder 2015). Furthermore, one of these reports suggested that the loss of CCR2 could improve the disease by regulating macrophage infiltration (Okuma et al. 2004). A study conducted by Groves et al. (2018) also showed that CCR2 knockout chimeric mice exposed to radiation had a reduced number of infiltrating monocytes and reduced pulmonary fibrosis compared to the wild type mice. Gillespie et al. (2010) found that both short term and long-term exposures to nickel hydroxide nanoparticles induced CCL2 in male mice and Morimoto et al. (2010) also reported that intratracheal instillation of nickel oxide nanoparticles induced CCL2/MCP-1 production in the male rats. Our findings show that NiNP-treated male mice had more CCL2 protein in BALF and whole lung lysates compared to females (Figure 9). This suggests that the increase in lung monocytic inflammation in male mice after subchronic exposure to NiNPs in the present study could be mediated by CCL2/CCR2 signaling. However, a caveat is that we observed the greatest increase in CCL2 induced by NiNPs alone, whereas the greatest increase in monocytes occurred in the NiNP and LPS co-exposure group (Figure 6). It is possible that CCL2 could have been increased earlier to signal monocyte influx and subsequently declined or other chemokines/mediators were contributory to monocyte influx. Also, lung mRNAs encoding CXCL1, IL-6, and CCL2 showed entirely different expression patterns compared to protein levels of these cytokines in BALF, with females having significant induction of all three cytokines after repeated, subchronic NiNP exposure (Supplementary File 2). These data reveal that mRNAs are not necessarily predictive of cytokine protein levels after repeated nanoparticle exposure.