Risk of gastrointestinal cancers from inhalation and ingestion of asbestos

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Abstract

This paper summarizes the weight of epidemiological evidence to evaluate the hypothesis that asbestos exposure is causally associated with increased risk of gastrointestinal (GI) cancers as suggested by Selikoff in an early study of insulation workers. This review looks at populations that develop GI cancers, namely stomach, colorectal, colon and rectal. Guidelines for assessing causality are strength of association, biological gradient and consistency of the associations. Exposure–response (E–R) was evaluated using three methods to estimate exposure. Rate Ratios (RRs) for lung cancer and percent of mesothelioma are used as surrogate measures of asbestos exposure for all the cohorts of exposed workers. Quantitative or semi-quantitative estimates of cumulative exposure to asbestos were also used to assess E–R trends and were compared to E–R trends for lung cancer and mesothelioma in individual studies. Surrogate measures are important since there are few individual studies that have assessed E–R. None of the various methods to estimate asbestos exposure yielded consistent E–R trends and the strength of the associations were consistently weak or non-existent for the four types of GI cancers. The epidemiological evidence detracts from the hypothesis that occupational asbestos exposure increases the risk of stomach, colorectal, colon, and rectal cancer. Findings are briefly summarized below.

Introduction

Selikoff et al., 1979, Selikoff et al., 1980 reported that among 632 building trades insulation workers with “light, intermittent exposure to asbestos” there was a 3-fold increased risk of GI cancers. Based on the 29 cancer cases, they concluded that the “data suggest that there may perhaps be an etiological relationship between industrial asbestos exposure and carcinoma of the gastrointestinal tract”. With 20 more years follow-up GI cancers still showed the 3-fold excess. Lung cancer showed a 7-fold increased risk at both time periods, while the occurrence of mesothelioma increased from 7% of total cancers to 18% during the follow-up.

Since then there have been a large number of mortality studies of asbestos workers and several reviews examining the associations of asbestos exposure and GI cancers. The conclusions are somewhat varied and range from a clear causal association to a lack of evidence to support the causal criteria or the presence of biased associations (Miller, 1978, Levine, 1985, Doll and Peto, 1985, Neugut and Wylie, 1987, Edelman, 1988, Frumkin and Berlin, 1991, Arbman et al., 1993, Homa et al., 1994, Gamble, 1994, Weiss, 1995, Goodman et al., 1999). The preponderance of the conclusions has been about colorectal cancer. But combining colon and rectal cancers might hide an association as suggested by Arbman et al. (1993). There have been fewer studies of stomach cancer, although in the follow-up study of the insulation cohort of Selikoff et al. (1979), stomach cancer showed an increased SMR and colorectal cancer a decreased SMR.

The purpose of this review is to evaluate the association between asbestos exposure and risk of stomach, colon and rectal cancers separately. The weight of the evidence from epidemiological studies will be graphically displayed so the causal criteria of strong association, exposure–response trends, and consistency can be evaluated. Known risk factors for these GI cancers will be briefly summarized to help identify potential confounders.

Section snippets

Study populations

A search of Toxline and Medline was conducted to identify cohort or case–control studies of asbestos-exposed workers where mortality or incidences of stomach, colon, rectal or colorectal cancers were analyzed. The references from individual studies and reviews were also searched for additional studies not obtained in the literature search. Cohorts or case control studies nested within asbestos-exposed cohorts will be the primary study populations included to be more certain of asbestos

Results

Results are presented individually for stomach cancer, colorectal cancer (CRC), colon and rectal cancer. The primary results are E–R trends presented in reverse order of importance: one figure each for surrogate E–R gradients (risk of lung cancer and mesothelioma) followed by variable numbers of graphs displaying E–R trends for individual studies.

Table 1 is a summary of the results from the 44 studies of asbestos-exposed workers included in this review. In Table 2, Table 3 the data from Table 1

Discussion

In general there are some findings of weak associations (RR < 1.5) at high surrogate exposures. Few studies evaluated individual-level E–R and in most instances there was a lack of E–R for the GI cancers while risk of lung cancer and mesothelioma consistently increased as exposure increased. There was a consistent lack of surrogate E–R trends. These patterns detract from the hypothesis that asbestos exposure causes GI cancer. The ingestion data consistently show no association with GI cancers but

Conflict of Interest

The author was employed at Exxon Mobil Biomedical Science Inc in Annandale, NJ while writing the draft manuscript.

Funding in Source

Funding was received from the International Environmental Research Foundation for presentation at the Taconite symposium and partial funding for writing the manuscript.

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