Toxic Metal Concentrations in Cigarettes Obtained from U.S. Smokers in 2009: Results from the International Tobacco Control (ITC) United States Survey Cohort

Caruso, Rosalie V.; O’Connor, Richard J.; Stephens, W. E.; Cummings, K. Michael; Fong, Geoffrey T.

doi:10.3390/ijerph110100202

Cited by 107 publications

(86 citation statements)

References 41 publications

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“…Torjussen et al (2003) indicated that nickel content is high in cigarettes, and it was in the range of 6.2-50.5 μg/L in the blood plasma of smokers [29]. Also, a study on US adult smokers (2009) reported that the mean value of nickel levels in cigarettes was 2.21 ± 0.54 μg per gram of tobacco [17]. Therefore, mothers' exposure to tobacco smoke can be one of the ways of entering nickel into the breast milk.…”

Section: Discussionmentioning

confidence: 94%

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The Nickel Concentration in Breast Milk during the First Month of Lactation in Yazd, Center of Iran

Salmani

Mozaffari‐Khosravi

Rezaei

2016

Biol Trace Elem Res

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Breastfeeding plays an important role in the growth and development of breastfed infants, especially in the first 6 months of their lives. The present study was conducted to determine the nickel concentrations in breast milk of lactating women in Yazd, Iran. One hundred fifty volunteers were selected among nursing mothers referring to health centers in Yazd. In the first month of lactation, milk samples were collected three times, on days 3 to 5 (first), 16 (Second), and 30 (third) after delivery. Nickel concentration of the samples was measured by atomic absorption spectrophotometer. Demographic variables were collected through a questionnaire which was completed by mothers. The mean age of the study group was 27.40 ± 4.66 years. The mean nickel concentrations in breast milk at the first, second, and third samples were 47.3 ± 7.40, 49.9 ± 8.05, and 54.8 ± 7.38 μg/l, respectively. The concentration of nickel in the breast milk of more than 86 % of mothers was higher than the permissible range for it. There was no significant relationship between the mean value of nickel in breast milk and education, age, and job of mothers. High level of nickel in breast milk may be attributed to consumed food and drinking water containing nickel. Monitoring the nickel level in breast milk regularly is recommended.

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Section: Discussionmentioning

confidence: 94%

“…Nickel toxicity studies on animals revealed the lipid peroxidation in the kidney, liver, and lung [17]. The data from human studies indicate that symptoms of acute exposure to nickel consist of gastro-intestinal disorders (nausea, vomiting, abdominal pain, and diarrhea), visual disturbance, headache, vertigo, and cough.…”

Section: Introductionmentioning

confidence: 96%

The Nickel Concentration in Breast Milk during the First Month of Lactation in Yazd, Center of Iran

Salmani

Mozaffari‐Khosravi

Rezaei

2016

Biol Trace Elem Res

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“…79 Cadmium has been shown to reduce CFTR expression via a miRNA dependent pathway, reducing channel function. Moreover, cadmium levels in lung were correlated with COPD disease severity independent of the duration of cigarette smoking.…”

Section: Mediators Of Cftr Dysfunction In Cigarette Smokementioning

confidence: 99%

Acquired Cystic Fibrosis Transmembrane Conductance Regulator Dysfunction in Chronic Bronchitis and Other Diseases of Mucus Clearance

Raju

Solomon

Dransfield

et al. 2016

Clinics in Chest Medicine

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Summary Chronic obstructive pulmonary disease (COPD) is a major public health problem accounting for more than 100,000 deaths and 750,000 hospitalizations each year in the United States alone. Though bronchodilators, inhaled steroids and other anti-inflammatory drugs can improve symptoms and reduce the risk of exacerbations, no therapies alter the natural history of the disease. This is the result of a number of factors including our poor understanding of the pathobiologic processes that drive specific COPD phenotypes, which has hindered drug development. Chronic bronchitis is perhaps the most clinically troublesome phenotype as most patients with COPD complain of cough and sputum production, and yet there are no effective treatments to target the mucus hypersecretion, accumulation and poor clearance that lead to these symptoms. Though it is well known that the absence of cystic fibrosis (CF) transmembrane receptor (CFTR) is the cause of CF, the prototypical disease of impaired mucociliary clearance, emerging data strongly suggest cigarette smoke and its components can lead to acquired CFTR dysfunction. Findings in vitro, in animal models, as well smokers with and without COPD also exhibit acquired CFTR dysfunction, which is associated with chronic bronchitis. This abnormality is not only present in the airways but is also present in extrapulmonary organs, suggesting CFTR dysfunction may contribute to smoking related lung disease as well as commonly associated comorbidities in which CFTR has a role. The development of potent CFTR modulators for the treatment of CF has made these findings clinically relevant as they may also have a role in treating COPD and other diseases of mucus clearance.

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“…Nickel concentrations in the air can reach high levels at industrial workplaces where it is used [4]. Additionally, nickel is present in cigarette smoke [5]. Inhalation exposure to nickel is associated with pulmonary inflammation, epithelial hyperplasia, fibrosis, asthma, and lung cancers [1,2,3].…”

Section: Introductionmentioning

confidence: 99%

Nickel inhibits mitochondrial fatty acid oxidation

Uppala

McKinney

Brant

et al. 2015

Biochemical and Biophysical Research Communications

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Nickel exposure is associated with changes in cellular energy metabolism which may contribute to its carcinogenic properties. Here, we demonstrate that nickel strongly represses mitochondrial fatty acid oxidation—the pathway by which fatty acids are catabolized for energy—in both primary human lung fibroblasts and mouse embryonic fibroblasts. At the concentrations used, nickel suppresses fatty acid oxidation without globally suppressing mitochondrial function as evidenced by increased glucose oxidation to CO2. Pre-treatment with L-carnitine, previously shown to prevent nickel-induced mitochondrial dysfunction in neuroblastoma cells, did not prevent the inhibition of fatty acid oxidation. The effect of nickel on fatty acid oxidation occurred only with prolonged exposure (>5 hr), suggesting that direct inhibition of the active sites of metabolic enzymes is not the mechanism of action. Nickel is a known hypoxia-mimetic that activates hypoxia inducible factor-1α (HIF1α). Nickel-induced inhibition of fatty acid oxidation was blunted in HIF1α knockout fibroblasts, implicating HIF1α as one contributor to the mechanism. Additionally, nickel down-regulated the protein levels of the key fatty acid oxidation enzyme very long-chain acyl-CoA dehydrogenase (VLCAD) in a dose-dependent fashion. In conclusion, inhibition of fatty acid oxidation by nickel, concurrent with increased glucose metabolism, represents a form of metabolic reprogramming that may contribute to nickel-induced carcinogenesis.

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Toxic Metal Concentrations in Cigarettes Obtained from U.S. Smokers in 2009: Results from the International Tobacco Control (ITC) United States Survey Cohort

Cited by 107 publications

References 41 publications

The Nickel Concentration in Breast Milk during the First Month of Lactation in Yazd, Center of Iran

The Nickel Concentration in Breast Milk during the First Month of Lactation in Yazd, Center of Iran

Acquired Cystic Fibrosis Transmembrane Conductance Regulator Dysfunction in Chronic Bronchitis and Other Diseases of Mucus Clearance

Nickel inhibits mitochondrial fatty acid oxidation

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