Occupational exposures and pancreatic cancer: a meta-analysis

Our plain-English summary of Occupational exposures and pancreatic cancer: a meta-analysis, by I.A. Ojajärvi, T.J. Partanen, A. Ahlbom, et al (Occupational and Environmental Medicine, 2000).

The study

• Authors: I.A. Ojajärvi, T.J. Partanen, A. Ahlbom, P. Boffetta, T. Hakulinen, N. Jourenkova, T.P. Kauppinen, M. Kogevinas, M. Porta, H.U. Vainio, E. Weiderpass, C.H. Wesseling
• Journal: Occupational and Environmental Medicine
• Published: 2000;57(5):316-24
• Type of article: Meta-analysis
• Cited by: 128 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Objectives: Consolidation of epidemiological data on pancreatic cancer and worksite exposures.

Methods: Publications during 1969-98 were surveyed. Studies without verified exposures were excluded. Meta-analyses were conducted on data from 92 studies covering 161 populations, with results for 23 agents or groups of agents. With a standard format, five epidemiologists extracted risk estimates and variables of the structure and quality of each study. The extracted data were centrally checked. Random meta-models were applied.

Results: Based on 20 populations, exposure to chlorinated hydrocarbon (CHC) solvents and related compounds was associated with a meta-risk ratio (MRR) of 1.4 (95% confidence interval (95% CI) 1.0 to 1.8). Nickel and nickel compounds were considered in four populations (1.9; 1.2 to 3.2). Excesses were found also for chromium and chromium compounds (1.4; 0.9 to 2.3), polycyclic aromatic hydrocarbons (PAHs) (1.5; 0.9 to 2.5), organochlorine insecticides (1.5; 0.6 to 3.7), silica dust (1.4; 0.9 to 2.0), and aliphatic and alicyclic hydrocarbon solvents (1.3; 0.8 to 2.8). Evidence on pancreatic carcinogenicity was weak or non-positive for the following agents: acrylonitrile (1.1; 0.0 to 6.2); arsenic (1.0; 0.6 to 1.5); asbestos (1.1; 0.9 to 1.5); diesel engine exhaust (1.0; 0.9 to 1.3); electromagnetic fields (1.1; 0.8 to 1.4); formaldehyde (0. 8; 0.5 to 1.0); flour dust (1.1; 0.3 to 3.2); cadmium and cadmium compounds (0.7; 0.4 to 1.4); gasoline (1.0; 0.8 to 1.2); herbicides (1.0; 0.8 to 1.3); iron and iron compounds (1.3; 0.7 to 2.5); lead and lead compounds (1.1; 0.8 to 1.5); man-made vitreous fibres (1.0; 0.6 to 1.6); oil mist (0.9; 0.8 to 1.0); and wood dust (1.1; 0.9 to 2.5). The occupational aetiological fraction of pancreatic cancer was estimated at 12%. In a subpopulation exposed to CHC solvents and related compounds, it was 29%; to chromium and chromium compounds, 23%; to nickel and nickel compounds, 47%; to insecticides, 33%; and to PAHs, 33%.

Conclusion: Occupational exposures may increase risk of pancreatic cancer. High quality studies are called for on interactions between occupational, environmental, and lifestyle factors as well as interactions between genes and the environment.

In plain English

This was a meta-analysis, pooling results from earlier published studies. The authors searched three databases for 1969 to May 1998 studies of pancreatic cancer and workplace exposures. They combined results from 92 studies covering 161 exposed populations, mostly in North America and Western Europe, for 23 agents including asbestos. Asbestos was not separated by fiber type. For asbestos, 24 populations gave a combined risk ratio of 1.1 (95% confidence interval 0.9 to 1.4). A rough statistical test showed significant variation between these studies. Twenty populations compared with general-population rates gave a statistically significant ratio of 1.2 (1.0 to 1.5), while four case-control populations gave 0.7 (0.5 to 1.0). The article's abstract lists asbestos among agents with weak or non-positive evidence. Statistically significant excesses were found for nickel and nickel compounds (1.9; 1.2 to 3.2) and chlorinated hydrocarbon solvents and related compounds (1.4; 1.0 to 1.8). The authors concluded that some chlorinated hydrocarbon solvents and related compounds may increase pancreatic cancer risk. They noted that too few studies adjusted for smoking to pool, and that death-certificate diagnoses are often wrong.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: meta-analysis of published epidemiological studies (cohort, case-control and other designs), using random effects models
• Who was studied: 92 published studies presenting data for 161 exposed populations, identified through Medline, Toxline and Cancerlit for 1969 to May 1998; 85 populations from North America and 63 from Western Europe; less than 5% of populations were women
• Exposure: 23 workplace agents or groups of agents, including asbestos (not divided by fiber type), nickel, chromium, chlorinated hydrocarbon solvents and related compounds, silica dust, man-made vitreous fibres and others; exposure was assessed mostly through job titles, expert assessment or job exposure matrices
• Main results:
  • Asbestos, all 24 populations combined (proportional studies excluded): meta-risk ratio 1.1 (95% CI 0.9 to 1.4); individual study estimates ranged from 0.5 to 3.6; p value for heterogeneity 0.004
  • Asbestos by study type: 20 populations compared with general-population rates (SMR/SIR studies) had a statistically significant meta-risk ratio of 1.2 (95% CI 1.0 to 1.5); 4 case-control populations had 0.7 (0.5 to 1.0)
  • Based on a rough statistical test, results varied significantly between studies for asbestos, as they did for electromagnetic fields, chlorinated hydrocarbon solvents and related compounds, and man-made vitreous fibres
  • In the article's abstract, asbestos is listed among agents for which evidence of pancreatic carcinogenicity was weak or non-positive
  • Statistically significant excesses: nickel and nickel compounds, meta-risk ratio 1.9 (1.2 to 3.2; four populations); chlorinated hydrocarbon solvents and related compounds, 1.4 (95% CI 1.0 to 1.8; 20 populations)
  • The overall share of pancreatic cancer attributed to workplace exposures was estimated at 12%. This share was not calculated for asbestos, because it was not calculated for agents with no indication of increased risk
• The authors' conclusion: The authors concluded that occupational exposure to some chlorinated hydrocarbon solvents and related compounds may increase the risk of pancreatic cancer. They wrote that excesses for chromium and nickel compounds were suggested, and that evidence was more limited for organochlorine insecticides, silica dust and aliphatic and alicyclic hydrocarbon solvents. Asbestos was not among the agents they named.
• Limitations the authors state:
  • Too few studies adjusted for smoking for their results to be pooled separately
  • Pancreatic cancer is often misdiagnosed, especially when the diagnosis comes only from death certificates; the authors say this biases the combined estimates toward no effect
  • Exposure assessment based on job titles, used in 57 populations, is of lower quality
  • SMR and SIR studies may be affected by the healthy worker effect, and the authors did not know how much this biased their results
  • The authors did not try to identify unpublished studies
  • The estimated shares of cancer attributable to exposures were unstable

Topics

Medical terms in this study, explained in our Lexicon: Occupational Exposure, Meta-Analysis, Consolidation, confidence interval, Vitreous.

Related studies

• Pancreatic cancer and occupational exposures — T. Kauppinen, T. Partanen, et al. (1995)
• Occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons and other agents and K-ras activation in human exocrine pancreatic cancer — J. Alguacil, M. Porta, et al. (2003)
• Exposure to environmental chemicals and heavy metals, and risk of pancreatic cancer — S.O. Antwi, E.C. Eckert, et al. (2015)
• Environmental risk factors for pancreatic cancer: an update — E. Barone, A. Corrado, et al. (2016)
• Assessment of "gene-environment" interaction in cases of familial and sporadic pancreatic cancer — T.P. Yeo, R.H. Hruban, et al. (2009)
• Slug enhances invasion ability of pancreatic cancer cells through upregulation of matrix metalloproteinase-9 and actin cytoskeleton remodeling — K. Zhang, D. Chen, et al. (2011)

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