Worker exposure to chemical agents in the manufacture of rubber tires and tubes: Particulates

Williams, Ted M.; Harris, Robert L.; Arp, Earl W.; Symons, Michael; Ert, Mark D. Van

doi:10.1080/15298668091424618

Cited by 20 publications

(6 citation statements)

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“…These calculations assume that 33.8% of the inhaled mass ends up in the pulmonary region [33] with a volume of inhaled air per hour of 1.8 L/h [36] and 8 h working days. CB exposure levels of up to 3.7 mg/m 3 , 2.2 mg/m 3 and 4.2 mg/m 3 have been reported for workers implicated in packaging and in handling CB [37-39]. BAL cell influxes revealed CBNP-induced inflammation that peaked 1 and 3 days post-exposure and persisted 28 days thereafter (Table 1).…”

Section: Discussionmentioning

confidence: 91%

Carbon black nanoparticle instillation induces sustained inflammation and genotoxicity in mouse lung and liver

et al. 2012

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BackgroundWidespread occupational exposure to carbon black nanoparticles (CBNPs) raises concerns over their safety. CBNPs are genotoxic in vitro but less is known about their genotoxicity in various organs in vivo.MethodsWe investigated inflammatory and acute phase responses, DNA strand breaks (SB) and oxidatively damaged DNA in C57BL/6 mice 1, 3 and 28 days after a single instillation of 0.018, 0.054 or 0.162 mg Printex 90 CBNPs, alongside sham controls. Bronchoalveolar lavage (BAL) fluid was analyzed for cellular composition. SB in BAL cells, whole lung and liver were assessed using the alkaline comet assay. Formamidopyrimidine DNA glycosylase (FPG) sensitive sites were assessed as an indicator of oxidatively damaged DNA. Pulmonary and hepatic acute phase response was evaluated by Saa3 mRNA real-time quantitative PCR.ResultsInflammation was strongest 1 and 3 days post-exposure, and remained elevated for the two highest doses (i.e., 0.054 and 0.162 mg) 28 days post-exposure (P < 0.001). SB were detected in lung at all doses on post-exposure day 1 (P < 0.001) and remained elevated at the two highest doses until day 28 (P < 0.05). BAL cell DNA SB were elevated relative to controls at least at the highest dose on all post-exposure days (P < 0.05). The level of FPG sensitive sites in lung was increased throughout with significant increases occurring on post-exposure days 1 and 3, in comparison to controls (P < 0.001-0.05). SB in liver were detected on post-exposure days 1 (P < 0.001) and 28 (P < 0.001). Polymorphonuclear (PMN) cell counts in BAL correlated strongly with FPG sensitive sites in lung (r = 0.88, P < 0.001), whereas no such correlation was observed with SB (r = 0.52, P = 0.08). CBNP increased the expression of Saa3 mRNA in lung tissue on day 1 (all doses), 3 (all doses) and 28 (0.054 and 0.162 mg), but not in liver.ConclusionsDeposition of CBNPs in lung induces inflammatory and genotoxic effects in mouse lung that persist considerably after the initial exposure. Our results demonstrate that CBNPs may cause genotoxicity both in the primary exposed tissue, lung and BAL cells, and in a secondary tissue, the liver.

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Section: Discussionmentioning

confidence: 91%

Carbon black nanoparticle instillation induces sustained inflammation and genotoxicity in mouse lung and liver

et al. 2012

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“…Most exposure surveys in the rubber industry have concentrated on airborne particulates and solvents. [41][42][43][44][45] However, for respiratory cancers, specific carcinogens such as asbestos and asbestos contaminated talc, polycyclic aromatic hydrocarbons, nitrosamines, and carbon black, used as a filler and reinforcing agent, 46 need to be considered. Measurements in the rubber industry are available for nitrosamines, 7-9 47 and to a lesser extent for polycyclic aromatic hydrocarbons and carbon black.…”

Section: Discussionmentioning

confidence: 99%

Workplace risk factors for cancer in the German rubber industry: Part 1. Mortality from respiratory cancers.

Weiland¹,

Straif²,

Chambless³

et al. 1998

Occup Environ Med

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Objectives-To determine the cancer specific mortality by work area among active and retired male workers in the German rubber industry. Methods-A cohort of 11 663 male German workers was followed up for mortality from 1 January 1981 to 31 December 1991. Cohort members were classified as active (n=7536) or retired (n=4127) as of 1 January 1981 and had been employed for at least one year in one of five study plants producing tyres or technical rubber goods. Work histories were reconstructed with routinely documented "cost centre codes" which were classified into six categories: I preparation of materials; II production of technical rubber goods; III production of tyres; IV storage and dispatch; V maintenance; and VI others. Standardised mortality ratios (SMRs) adjusted for age and calendar year and 95% confidence intervals (95% CIs), stratified by work area (employment in respective work area for at least one year) and time related variables (year of hire, lagged years of employment in work area), were calculated from national reference rates. Results-SMRs for laryngeal cancer were highest in work area I (SMR 253; 95% CI 93 to 551) and were significant among workers who were employed for >10 years in this work area (SMR 330; 95% CI 107 to 779). Increased mortality rates from lung cancer were identified in work areas I (SMR 162; 95% CI 129 to 202), II (SMR 134; 95% CI 109 to 163), and V (SMR 131; 95% CI 102 to 167). Mortality from pleural cancer was increased in all six work areas, and significant excesses were found in work areas I (SMR 448; 95% CI 122 to 1146), II (SMR 505; 95% CI 202 to 1040), and V (SMR 554; 95% CI 179 to 1290). Conclusion-A causal relation between the excess of pleural cancer and exposure to asbestos among rubber workers is plausible and likely. In this study, the pattern of excess of lung cancer parallels the pattern of excess of pleural cancer. This points to asbestos as one risk factor for the excess deaths from lung cancer among rubber workers. The study provides further evidence for an increased mortality from laryngeal cancer among workers in the rubber industry, particularly in work area I. (Occup Environ Med 1998;55:317-324)

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“…'7 18 Environmental exposure in final inspection-tyres is primarily to particulates resulting from the buffing and grinding of the cured products. 17 Several rubber chemicals may possibly generate aromatic amines. Chief among these are N-nitrosodiphenylamine, diphenylamine, aldol-alpha-naphthylamine, phenyl-alpha-and phenyl-beta-naphthylamine (PBNA).…”

Section: Discussionmentioning

confidence: 99%

A case-control study of bladder cancer in the United States rubber and tyre industry.

Checkoway¹,

Smith²,

McMichael³

et al. 1981

Occupational and Environmental Medicine

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Worker exposure to chemical agents in the manufacture of rubber tires and tubes: Particulates

Cited by 20 publications

References 0 publications

Carbon black nanoparticle instillation induces sustained inflammation and genotoxicity in mouse lung and liver

Carbon black nanoparticle instillation induces sustained inflammation and genotoxicity in mouse lung and liver

Workplace risk factors for cancer in the German rubber industry: Part 1. Mortality from respiratory cancers.

A case-control study of bladder cancer in the United States rubber and tyre industry.

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