Silicosis and end-stage renal disease

Steenland, Kyle; Rosenman, Ken; Socie, Ed; Valiante, Dave

doi:10.5271/sjweh.696

Cited by 20 publications

(19 citation statements)

References 13 publications

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“…Unfortunately, this type of specificity is rarely found on death certificates, thus, the need to link silica exposure with incidence end-stage renal disease registries. (9) In this regard, Steenland et al (7) examined end-stage renal disease incidence with silica exposure. Incidence was determined by record linkage to a national registry of treated end-stage renal disease patients.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Cohort Mortality Study of Roofing Granule Mine and Mill Workers. Part II. Epidemiologic Analysis, 1945–2004

Olsen

Andres

Johnson

et al. 2012

Journal of Occupational and Environmental Hygiene

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The mortality of 2650 employees (93.4% males) in the mine and mill production of roofing granules at four plants was examined between 1945 and 2004. Hypotheses focused on diseases associated with exposure to silica: nonmalignant respiratory disease, lung cancer, and nonmalignant renal disease. Study eligibility required ≥ 1 year of employment by 2000. Work history and vital status were followed through 2004 with < 1% lost to follow-up. Industrial hygiene sampling data (1871 sampling measurements over a 32-year period) and professional judgment were used to construct 15 respirable crystalline silica exposure categories. A category was assigned to all plant-, department-, and time-dependent standard job titles. Cumulative respirable crystalline silica exposure (mg/m(3)-years) was calculated as the sum of the product of time spent and the average exposure for each plant-, department-, job-, and calendar-year combination. The cohort geometric mean was 0.17 mg/m(3)-years (geometric standard deviation 4.01) and differed by plant. Expected deaths were calculated using U.S. (entire cohort) and regional (each plant) mortality rates. Poisson regression was used for internal comparisons. For the entire cohort, 772 deaths (97.4% males) were identified (standardized mortality ratio 0.95, 95% CI 0.88-1.02). There were 50 deaths from nonmalignant respiratory diseases (1.14, 95% CI 0.85-1.51). Lagging exposure 15 years among the male cohort, the relative risks for nonmalignant respiratory disease were 1.00 (reference), 0.80, 1.94, and 2.03 (p value trend = 0.03) when cumulative exposure was categorized < 0.1, 0.1- < 0.5, 0.5- < 1.0, and ≥ 1.0 mg/m(3)-years, respectively. There was a total of 77 lung cancer deaths (1.11, 95% CI 0.88-1.39). Lagging exposure 15 years, the relative risks for males were 1.00 (reference), 1.83, 1.83, and 1.05 (p value trend = 0.9). There were 16 deaths from nonmalignant renal disease (1.76, 95% CI 1.01-2.86). This exposure-response trend was suggestive but imprecise. The study results are consistent with other cohorts with similar levels of exposure to respirable crystalline silica.

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Section: Discussionmentioning

confidence: 99%

“…(6) In several occupational cohort mortality studies of workers exposed to silica, an excess of deaths from nonmalignant renal disease has been reported, (7)(8)(9) although not consistently. (10,11) These findings have been attributed to the possibility of silicaassociated immune complexes deposited in the kidneys.…”

Section: Introductionmentioning

confidence: 99%

Cohort Mortality Study of Roofing Granule Mine and Mill Workers. Part II. Epidemiologic Analysis, 1945–2004

Olsen

Andres

Johnson

et al. 2012

Journal of Occupational and Environmental Hygiene

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“…Recent studies have focused on the toxicology of SiO 2 NPs and have found that SiO 2 NPs can cause harmful biological responses in diverse organs. [4][5][6][7][8][9] The liver, as the major organ for the biotransformation of toxins, is a primary target organ for nanoparticles.…”

Section: Introductionmentioning

confidence: 99%

Kupffer cell-mediated hepatic injury induced by silica nanoparticles in vitro and in vivo

Chen¹,

Yang²,

Sun³

2013

IJN

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Silica nanoparticles (SiO 2 NPs) have been shown to exert cytotoxic effects in hepatocytes and to cause liver injury. In the liver, Kupffer cells (KCs), as the resident macrophages, play an important role in the normal physiology and homeostasis of the liver. Nevertheless, few studies have attempted to clarify the role of KCs in hepatic injury induced by SiO 2 NPs. In this study, we treated Buffalo rat liver (BRL) cells with the supernatants of SiO 2 NP-stimulated KCs to determine KC-mediated hepatotoxicity and its underlying preliminary mechanism. We also examined the response of KCs and liver injury in vivo after the administration of SiO 2 NPs. The results showed that KCs stimulated by SiO 2 NPs release large amounts of reactive oxygen species, tumor necrosis factor-α and nitric oxide. After BRL cells were cultured with the supernatants of SiO 2 NP-stimulated KCs, the viability of BRL cells was reduced, and increases in aspartate aminotransferase and lactate dehydrogenase leakage were observed. Exposure to SiO 2 NPs in vivo caused KC hyperplasia, hepatic inflammation, and oxidative stress, which led to changes in the biochemical composition of the liver. These data suggest that SiO 2 NPs activate KCs to mediate hepatic injury and that the preliminary mechanism involves the release of bioactive substances from KCs.

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“…For example, in one analysis of data from 3 existing cohort studies, Steenland and colleagues observed that individuals who were exposed to silica had a 5.1% excess risk of end-stage renal disease (ESRD) and a 1.8% excess risk of death from kidney disease 11 . The mechanisms by which silica may damage the renal system can be either through direct (silica particles in the kidney) or indirect toxicity 13 . This indirect toxicity likely occurs when the lungs, after being exposed to silica particles, begin to produce macrophages to attack the particles.…”

Section: Introductionmentioning

confidence: 99%

Occupational Silica Exposure and Chronic Kidney Disease

et al. 2011

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Introduction Occupational exposure to silica may be associated with chronic kidney disease (CKD). Most studies have been conducted in occupational cohorts with high levels of exposure but small numbers of cases. We analyzed data from a population-based case-control study of occupational silica exposure and CKD. Methods Cases were hospital patients with newly diagnosed CKD and community controls were selected using random digit dialing and frequency matched by age, gender, race and proximity to the hospital. Silica exposure estimates were assigned by industrial hygiene review of lifetime job history data and weighted for certainty and intensity. Conditional logistic regression was used to estimate the odds ratios (ORs) for CKD conditioned on demographic, lifestyle and clinical variables. Results The mean age of participants was 62 years (range, 30-83 years), 56% were male and 54% were white. Any silica exposure (compared to none) was associated with a 40% increased risk of CKD (OR=1.40, 95% confidence interval [CI]: 1.04, 1.89) in a multivariable adjusted model. The mean cumulative duration of silica exposure was significantly higher in exposed cases than in exposed controls (33.4 vs. 24.8 years, respectively). Overall, compared to non-exposed participants, the ORs (95% CI) for those below and above the median duration of silica exposure were 1.20 (95% CI: 0.77, 1.86) and 1.76 (95% CI: 1.14, 2.71), respectively. Conclusions We found a positive relationship between occupational silica exposure and CKD. A dose-response trend of increasing CKD risk with increasing duration of silica exposure was observed and was particularly strong among non-whites.

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Silicosis and end-stage renal disease

Cited by 20 publications

References 13 publications

Cohort Mortality Study of Roofing Granule Mine and Mill Workers. Part II. Epidemiologic Analysis, 1945–2004

Cohort Mortality Study of Roofing Granule Mine and Mill Workers. Part II. Epidemiologic Analysis, 1945–2004

Kupffer cell-mediated hepatic injury induced by silica nanoparticles in vitro and in vivo

Occupational Silica Exposure and Chronic Kidney Disease

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