Identification of occupational cancer risk in British Columbia: A population‐based case–control study of 2,998 lung cancers by histopathological subtype

MacArthur, Amy C.; Le, Nhu D.; Fang, Raymond; Band, Pierre R.

doi:10.1002/ajim.20663

Cited by 22 publications

(11 citation statements)

References 41 publications

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“…Our findings are consistent with those of previous studies suggesting that occupational exposure to PACs, in particular asphalt and tar and automobile exhaust, may increase risk of lung cancer (Boffetta et al, 2003a; Boffetta et al, 2003b; Bosetti et al, 2007; Garshick et al, 2008; MacArthur et al, 2009). Most notably, Boffetta et al (2003b) conducted a multi-country study of 29,820 male asphalt workers from eight European countries with mortality that was documented from 1953 to 2000.…”

Section: Discussionsupporting

confidence: 93%

A case–control study of asphalt and tar exposure and lung cancer in minorities

McClean¹,

Kelsey²,

Sison³

et al. 2011

American J Industrial Med

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Objectives Considerable controversy surrounds the carcinogenic potential of asphalt and tar. Since minority individuals may have had relatively high historical exposures, we investigated asphalt and tar exposure and lung cancer risk among African Americans and Latino Americans. Methods We conducted a case-control study of lung cancer among African Americans and Latino Americans in the San Francisco Bay area (422 cases, 894 controls). A questionnaire was used to obtain detailed work histories and exposure information. Self-reported exposure to asphalt and tar as well as other factors (eg. smoking, automobile exhaust, and asbestos) were evaluated as predictors of lung cancer risk. Potential effect modification by cytochrome P450 (CYP) 1A1 was also explored. Results Self-reported duration of exposure to asphalt and tar was associated with a statistically significant excess risk of lung cancer in the overall population (OR: 1.11, 95%CI: 1.01–1.22), evaluating risk per year of exposure. Years of exposure to automobile exhaust (OR: 1.02, 95%CI: 1.00–1.05) and asbestos (OR: 1.04, 95%CI: 1.02–1.06) were also associated with statistically significant elevations in risk. In Latino Americans, the lung cancer risks associated with polycyclic aromatic hydrocarbon-related exposures were consistently higher in the CYP1A1 wildtype subjects as compared to the variant genotype subjects, and the interaction was statistically significant for smoking and the CYP1A1 M2 polymorphism (p-valueinteraction=0.02). Conclusions These data are consistent with the literature suggesting that exposure to asphalt and tar may increase risk of lung cancer. However, it was not possible to separate the effects and asphalt and tar in this study.

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Section: Discussionsupporting

confidence: 93%

A case–control study of asphalt and tar exposure and lung cancer in minorities

McClean¹,

Kelsey²,

Sison³

et al. 2011

American J Industrial Med

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“…Increased risks of lung cancer have already been reported for occupations in the metal industry [Morabia et al, 1992; Bruske‐Hohlfeld et al, 2000; Matos et al, 2000; Bardin‐Mikolajczak et al, 2007; MacArthur et al, 2009; Yenugadhati et al, 2009]. These occupations can entail exposure to asbestos, a well‐known lung carcinogen, but also to potentially carcinogenic metal fumes and dust (e.g., arsenic, chromium) [IARC, 1990; Siemiatycki et al, 2004].…”

Section: Discussionmentioning

confidence: 99%

Lung cancer and occupation: A new zealand cancer registry‐based case–control study

Corbin

McLean

Mannetje

et al. 2010

American J Industrial Med

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“…Although wide strata of the general population are exposed to low, background levels of toxic and carcinogenic inhalable compounds, industrial workers have been often exposed to significantly higher concentrations of potentially carcinogenic agents released from multiple sources (MacArthur et al 2009). Foundry work is a specific condition of exposure to inhalable metal-rich PM that has been associated with increased risk of lung cancer in several early investigations (International Agency for Research on Cancer 1987).…”

mentioning

confidence: 99%

Inhalable Metal-Rich Air Particles and Histone H3K4 Dimethylation and H3K9 Acetylation in a Cross-sectional Study of Steel Workers

Cantone

Nordio

Hou³

et al. 2011

Environ Health Perspect

144

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Background: Epidemiology investigations have linked exposure to ambient and occupational air particulate matter (PM) with increased risk of lung cancer. PM contains carcinogenic and toxic metals, including arsenic and nickel, which have been shown in in vitro studies to induce histone modifications that activate gene expression by inducing open-chromatin states. Whether inhalation of metal components of PM induces histone modifications in human subjects is undetermined.Objectives: We investigated whether the metal components of PM determined activating histone modifications in 63 steel workers with well-characterized exposure to metal-rich PM.Methods: We determined histone 3 lysine 4 dimethylation (H3K4me2) and histone 3 lysine 9 acetylation (H3K9ac) on histones from blood leukocytes. Exposure to inhalable metal components (aluminum, manganese, nickel, zinc, arsenic, lead, iron) and to total PM was estimated for each study subject.Results: Both H3K4me2 and H3K9ac increased in association with years of employment in the plant (p-trend = 0.04 and 0.006, respectively). H3K4me2 increased in association with air levels of nickel [β = 0.16; 95% confidence interval (CI), 0.03–0.3], arsenic (β = 0.16; 95% CI, 0.02–0.3), and iron (β = 0.14; 95% CI, 0.01–0.26). H3K9ac showed nonsignificant positive associations with air levels of nickel (β = 0.24; 95% CI, –0.02 to 0.51), arsenic (β = 0.21; 95% CI, –0.06 to 0.48), and iron (β = 0.22; 95% CI, –0.03 to 0.47). Cumulative exposures to nickel and arsenic, defined as the product of years of employment by metal air levels, were positively correlated with both H3K4me2 (nickel: β = 0.16; 95% CI, 0.01–0.3; arsenic: β = 0.16; 95% CI, 0.03–0.29) and H3K9ac (nickel: β = 0.27; 95% CI, 0.01–0.54; arsenic: β = 0.28; 95% CI, 0.04–0.51).Conclusions: Our results indicate histone modifications as a novel epigenetic mechanism induced in human subjects by long-term exposure to inhalable nickel and arsenic.

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Identification of occupational cancer risk in British Columbia: A population‐based case–control study of 2,998 lung cancers by histopathological subtype

Abstract: Our results point to excess lung cancer risk for occupations involving exposure to metals, polyaromatic hydrocarbons and asbestos, as well as several new histopathologic-specific associations that merit further investigation.

Cited by 22 publications

References 41 publications

A case–control study of asphalt and tar exposure and lung cancer in minorities

A case–control study of asphalt and tar exposure and lung cancer in minorities

Lung cancer and occupation: A new zealand cancer registry‐based case–control study

Inhalable Metal-Rich Air Particles and Histone H3K4 Dimethylation and H3K9 Acetylation in a Cross-sectional Study of Steel Workers

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